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Escherichia coli cells contain potential division sites at midcell and adjacent to the cell poles. Selection of the correct division site at midcell is controlled by three proteins: MinC, MinD, and MinE. It has previously been shown (D. Raskin and P. de Boer, Cell 91:685–694, 1997) that MinE-Gfp localizes to the midcell site in an MinD-dependent manner. We use here Gfp-MinD to show that MinD associates with the membrane around the entire periphery of the cell in the absence of the other Min proteins and that MinE is capable of altering the membrane distribution pattern of Gfp-MinD. Studies with the isolated N-terminal and C-terminal MinE domains indicated different roles for the two MinE domains in the redistribution of membrane-associated MinD.
Cell division in Escherichia coli and most other rod-shaped bacteria occurs by formation of a division septum at the midpoint of the cell, thus ensuring the equipartition of cytoplasmic components into the two daughter cells. To ensure that division occurs only at the midcell site, the cell must select this site in preference to other potential division sites that are located adjacent to the cell poles. If the polar sites are used to support septum formation, small chromosomeless minicells are formed that are incapable of undergoing further divisions. In E. coli, the selective suppression of the polar division sites is accomplished by the cooperative action of the three gene products of the minCDE locus: MinC, MinD, and MinE.
Previous studies (4) have shown that the three Min proteins act in the following way. MinC and MinD act in concert to form a nonspecific inhibitor of septation. In this process, MinD functions to activate the latent division inhibitory activity of MinC (6). The MinCD division inhibitor lacks site specificity, as shown by the observation that expression of minC andminD in the absence of minE leads to a block in septation at all potential division sites, leading to formation of long nonseptate filaments. Filamentation is suppressed by MinE, which acts as a topological specificity factor to prevent the division inhibitor from acting at the midcell site while permitting it to block septation at polar division sites.
The ability of MinE to counteract the MinCD division inhibitor and the ability to impart topological specificity to the system reside in different domains of the 88-amino-acid MinE protein. The N-terminal MinE domain is responsible for the anti-MinCD function, as shown by the ability of MinE1–22 (20) or MinE1–34 (13) to prevent MinCD-induced filamentation. (Superscripts [e.g., minE1–53] refer to amino acid positions within MinE or within the minEgene product.) The C-terminal domain of MinE is thought to encode the MinE topological specificity function that is responsible for limiting its action to the division site at midcell. It has been proposed that topological specificity is accomplished by the binding of the C-terminal topological specificity domain to a putative topological target molecule at the new division site at midcell (17). The sequestration of MinE at midcell would permit it to interfere with the division inhibitor at this site without interfering with the division inhibition activity at the unwanted polar division sites. As a result, normal cell division would occur and polar divisions would be prevented. Excess MinE has been shown to induce minicell formation, suggesting that once the topological target is saturated, the excess MinE molecules are free to counteract the division inhibitor elsewhere in the cell.
Consistent with the ability of MinE to specifically counteract the division inhibitor at midcell, a MinE-green fluorescent protein chimera (MinE-Gfp) localizes to a ring-like structure at sites adjacent to the midcell, and this localization pattern requires the simultaneous expression of minD (14). This implicates MinD in the process that leads to localization of MinE at midcell.
MinD plays several roles in the Min system. First, it activates the MinC division inhibitor. Second, it is required to make the division inhibitor sensitive to MinE (5, 10). Third, MinD is required to localize MinE at midcell (14). After the initial submission of the present study for publication, it was shown in a related study that MinD localizes to the cell pole in a MinE-dependent fashion and undergoes a rapid oscillation from pole to pole (16).
We have also examined the cellular localization of the MinD protein and its membrane interactions with MinE by using a green fluorescent protein-MinD fusion protein (Gfp-MinD) to monitor the cellular distribution of MinD. In this report we describe the membrane rearrangements of Gfp-MinD that are induced by coexpression with MinE, and we define a specific role for the N-terminal MinE domain in this process.
Bacterial strains. E. coli PB114 (λDB217) was derived from PB114 (ΔminCDE) (4) and λDB217 (Plac-minC). λDB217 was constructed by in vivo recombination of plasmid pDB217 (6) with λNT5 (3). E. coli RC1 [ΔminCDEΔ(araAB01C-leu)] was constructed by P1-mediated transduction of Δmin from PB114 into E. coliMC1000.
Plasmids.pSY1057 (Plac-minE22–88), a pUC derivative, has been previously described (19). pJPB262 (Plac-minE1–32) was a gift from Jean-Pierre Bouché (13); this pUC8-derived plasmid contains a termination codon immediately afterminE1–32 and theminE33–88 portion of minE has been deleted.
For pSY1053 (Plac-minE1–53), theHindIII/XbaI fragment from pZC20 (20), in which a translational stop codon followsminE1–53, was subcloned into pBluescript KS (Stratagene). For pDB188 (Plac-minE), theHindIII/EcoRI fragment from pDB156 (4) was inserted intoHindIII/EcoRI-digested pBluescript KS. For pAS72, NdeI/HindIII-digested pET21a (Novagen) was ligated to a fragment containing the minD gene from pDB175 (4), prepared by PCR; the fragment lacks anyminE sequences. For pAS74 (Plac-minD), theXbaI/HindIII minD fragment from pAS72 was inserted into XbaI/HindIII-digested pBluescript SK. For pFX1 (Plac-minE1–53::gfp), pDB175 (4) was used as template in a PCR reaction to generate a minE fragment coding for amino acids 1 to 53, preceded by the terminal region of minD that includes the ribosome-binding site for minE translation; PCR was also used to generate a fragment from pKENgfpmut2 (1) that includes the entire gfpmut2 gene, immediately preceded by aBamHI site. The two fragments were cleaved withEcoRI/BamHI andBamHI/HindIII, respectively, and the fragments were ligated intoEcoRI/HindIII-digested pBluescript. The resulting pFX1 plasmid contains minE1–53 cloned in frame to gfpmut2, with an intervening four amino acid linker (Gly-Ser-Glu-Phe). For pFX11 (Plac-gfp::minD minE1–53), a minE1–53fragment with a TAG termination codon immediately after codon 53 was generated by PCR with pSLR23 as a template. The PCR fragment was cleaved with EcoRI/HindIII and ligated intoEcoRI/HindIII-digested pMLB1113 (4). The minE1–53-gfpfusion was verified by sequencing. pYW3 (Plac-minC gfp::minD minE) was constructed by ligating the 1.9-kbp HindIII (Klenow enzyme-treated)/NheI fragment from pSLR23, which containsgfp::minD minE, into pDB217 (Plac-minC) (6) that had been digested with XbaI (Klenow-treated) and SpeI.
The following plasmids were derived from the pACYC-derived plasmid pBAD33 (8) or pSJ4, a plasmid (kindly provided by S. Justice) that was derived from pBAD33 by site-directed mutagenesis that destroyed the EcoRI site in the cat gene without inactivating chloramphenicol resistance. pAS73 (Para-minD) encodes minD preceded by the ribosome-binding site and leader sequence of pET21a (Novagen). The plasmid was constructed by subcloning theXbaI/HindIII fragment from pAS72 intoXbaI/HindIII-digested pBAD33. pAS86 (Para-minE::gfp) contains minE fused in frame to gfpmut2; theminE::gfpmut2 fragment was originally prepared by PCR from pKEN1gfpmut2 (1) and was transferred toSmaI/HindIII-digested pBAD33 as anXmnI/HindIII fragment from the intermediate plasmid pAS82 (Para-minD minE::gfpmut2). pSLR21 (Para-gfpmut2) encodes thegfpmut2 gene, preceded by the ribosome-binding site and leader sequence of pET21a (Novagen). The plasmid was constructed by ligating a PCR-derived gfpmut2-containing fragment toEcoRI/HindIII-digested pSJ4, thereby placinggfpmut2 under Para control. The fragment was derived by PCR with a pKEN derivative encoding thegfpmut2 gene (1) as a template. pSLR22 (Para-gfpmut2::minD) encodes the gfpmut2 gene fused in frame to the 5′ end of theminD gene and preceded by the ribosome-binding site and leader sequence of pET21a. The stop codon of gfp was replaced with a tyrosine codon. In the protein product, Gfp is linked to MinD by a Gly-Ser-Arg-Phe linker which also encodes anXbaI site, and Met-1 of MinD has been replaced by Ile. This protein can be produced at a high concentration without the formation of inclusion bodies. The plasmid was constructed by ligatingEcoRI/HindIII-digested pSJ4 to anEcoRI/XbaI-digested gfpmut2-containing fragment and an XbaI/HindIII-digestedminD-containing fragment. The gfpmut2 gene was obtained via PCR by using the same primers and template as for pSLR21; the minD gene was obtained by PCR with pDB175 as a template. The entire fusion gene was sequenced to ensure it was correct. pSLR23 (Para-gfpmut2::minD minE) encodes the same gfpmut2::minD fusion as pSLR22, upstream of the minE gene; the DNA sequence between minD and minE is as found on the E. coli chromosome. The plasmid was constructed by ligatingEcoRI/HindIII-digested pSJ4 to anEcoRI/XbaI-digested PCR product encodinggfpmut2 and to anXbaI/HindIII-digested minD minEPCR product derived from pDB175. The primers and template forgfpmut2 were the same as for pSLR22 (above). The entire PCR-generated insert was sequenced to ensure it was correct. pSLR24 (Para-minD minE) encodes the wild-typeminD and minE genes in tandem preceded by the ribosome-binding site and leader sequence of pET 21a. It was constructed by ligatingEcoRI/HindIII-digested pSJ4 to anEcoRI/HindIII-digested PCR product encoding minD minE, derived from plasmid pDB175 (4).
Growth conditions.Strains were grown overnight on L agar plates containing 1% glucose and antibiotics needed for plasmid maintenance (50 or 100 μg of ampicillin per ml for pUC or pBluescript-derived plasmids and 20 μg of chloramphenicol per ml for pBAD33-derived plasmids) and were inoculated the next morning into L broth containing the same additives. After 3 to 4 h of growth at 37°C, the cells were collected by centrifugation, washed twice with L broth, and suspended at an A600 of 0.04 in fresh L broth lacking glucose but containing antibiotics and inducer, where indicated. Unless otherwise stated, genes underPara control were expressed by growth in 0.001 to 0.005% arabinose, while genes under Placcontrol were expressed at basal levels by growth in the absence of IPTG (isopropyl-β-d-thiogalactopyranoside). The cultures were incubated with shaking at 30°C for 4 to 4.5 h, and cells were sampled directly from the culture for microscopy (unfixed) or were fixed by addition to the culture of 1.7% formaldehyde and 0.17% glutaraldehyde (final concentrations), followed by incubation at room temperature for 45 min. The fixed cells were collected by centrifugation, resuspended in 0.9% saline, and stored at 4°C until microscopic examination. Western blot analysis showed that the concentrations of Gfp-MinD in ΔminCDE cells containing plasmid pSLR22 (Para-gfp::minD), in cells grown for 4.5 h in the presence of 0.001 or 0.0025% arabinose, were 0.96- and 1.78-fold the concentration of MinD in the wild-type strain, respectively. In ΔminCDE cells containing plasmid pSLR23 (Para-gfp::minD minE) and grown in the presence of 0.001 or 0.0025% arabinose, the concentrations of Gfp-MinD were 1.17- and 2.1-fold and the concentrations of MinE were 5.0- and 9.5-fold, respectively, their concentrations in the wild-type strain.
Gel electrophoresis and immunoblotting.Cells for Western blot analysis were harvested by centrifugation and frozen immediately. Frozen samples were thawed by resuspension in sodium dodecyl sulfate-polyacrylamide gel electrophoresis loading buffer, boiled for 5 min, and subjected to sodium dodecyl sulfate-gel electrophoresis (11). Immunoblots were performed as previously described by using antibodies directed against MinE2–19 to compare the concentrations of MinE and N-terminal MinE fragments and antibody directed against a mixture of MinE29–38 and MinE70–88 to detect MinE+ or to compare the concentrations of MinE and of MinE C-terminal fragments (19, 20). Antibody raised against whole wild-type MinD protein was used to detect MinD and Gfp-MinD. Bands in Western blots were quantitated by using the ImageQuant program (Molecular Dynamics) on digitized images by using concentrations of cell extracts where the band intensity was proportional to amount of the sample applied to the gel.
Microscopy and data analysis.Samples were examined by phase contrast, Nomarski, and fluorescence microscopy. A minicell phenotype was defined by the presence of moderate to large numbers of spherical minicells, polar septa, and cells with a length ranging from the wild-type length to short filaments of approximately four to six cell lengths. A filamenting phenotype was defined by the virtual to complete absence of minicells and by the presence of large numbers of filaments, ranging from 6 to 100 cell lengths. Fluorescence images were collected by using an integrating charge-coupled device camera. Measurements of cell lengths and positions of cell landmarks and data analysis were done by using the public domain NIH Image program (http://rsb.info.nih.gov/nih-image/ ) and in-house software.
Phenotypic effects of a Gfp-MinD fusion protein.To study the cellular localization of MinD, we constructed agfp::minD fusion that codes for a protein (Gfp-MinD) in which the high quantum yield Gfpmut2 (1) (called Gfp in the remainder of this study) is fused to the N-terminal end of MinD. Thegfp::minD fusion was expressed under control of the arabinose-inducible BAD promoter to permit coexpression of other relevant genes under Plac control in the same cell.
MinD normally performs two functions that affect formation of the division septum and that can be assayed in vivo: (i) MinD is an activator of the MinC division inhibitor and (ii) MinD makes the division inhibitor sensitive to suppression by MinE. Evidence that the Gfp-MinD fusion protein retained these two functions was obtained by comparing the effects of MinD and Gfp-MinD on the division pattern of a Δmin strain in the presence of MinC and/or MinE.
As previously reported (4), induction of minCfrom an integrated Plac-minC prophage in the absence of MinD failed to block division in a ΔminCDEstrain (Fig. 1a), whereas coexpression ofminC and minD led to the formation of nonseptate filaments (Fig. 1b and c). Coexpression of minC andgfp::minD also induced filamentation when Plac-minC andPara-gfp::minD were coinduced by growth in the presence of IPTG and arabinose (Fig. 1d). We conclude that Gfp-MinD retained the MinC activation effect of MinD.
MinD is required to make MinC-mediated division inhibition sensitive to suppression by MinE (6). To ask whether Gfp-MinD retained this aspect of MinD function, minD orgfp::minD was expressed in cis with minE in cells that expressed minCfrom a Plac-minC λ prophage. As previously described, the expression of minE suppressed the filamentation that occurred when minC and minDwere coexpressed in the absence of minE (Fig. 1e). Similarly, filamentation was suppressed when minD was replaced by gfp::minD (in pSLR23, Fig.1f). Thus, Gfp-MinD behaves similarly to MinD in making the activated MinC division inhibitor sensitive to MinE.
Raskin and de Boer (16) have shown that Gfp-MinD can correct the minicelling phenotype of a minD1 mutant, in which the mutation is located near the carboxy terminus of MinD (10). This showed that the Gfp-MinD protein retains the MinD function that is lost due to the minD1 mutation. In the present study, evidence that Gfp-MinD could provide all of the functions of MinD was obtained by expressing minC,gfp::minD, and minE in a ΔminCDE strain (from PB114/pYW3 [ΔminCDE/Plac-minC gfp::minD minE]). As illustrated in Fig. 1g, low-level derepression of Plac by growth of PB114/pYW3 in 0.005% or 0% glucose or 10 μM IPTG led to almost complete disappearance of the minicell phenotype. Similar results were obtained with wild-type MinD, expressed from pDB170 (Plac-minC minD minE) (data not shown) (4). In this case, minicelling was corrected at even lower levels of derepression, obtained by growth in 0.05 or 0.01% glucose. We conclude that Gfp-MinD has retained all of the important functions of MinD, although the Gfp moiety may interfere somewhat with MinD efficiency or stability.
Pattern of membrane-associated Gfp-MinD in the absence of MinE.It has previously been shown that MinE-Gfp can localize to sites near midcell and that this localization requires the presence of the MinD protein (14). We therefore studied the localization pattern of Gfp-MinD in the presence or absence of MinE. Experiments were performed in the Δmin strain PB114. Because of the Δmin background, the cells showed a minicell phenotype consisting of minicells plus cells ranging from wild-type cell length to short filaments. Cells were examined after low-level induction of Gfp-MinD fromPara-gfp::minD by growth in the presence of 0.001 to 0.005% arabinose. Under these conditions the phenotype of the Δmin host was unchanged.
Most fluorescent cells in the population showed a peripheral pattern of fluorescence that extended entirely around the cell (Fig.2a). The pattern was seen at all levels of arabinose induction that were tested. The peripheral pattern was not an optical artifact since expression of Gfp alone, in the absence of the MinD moiety, showed only diffuse cellular fluorescence without evidence of peripheral localization (Fig. 2b). We conclude that MinD can associate with the cell membrane around the entire periphery of the cell in the absence of other Min proteins, an idea consistent with the results of Raskin and de Boer (16).
In addition to the peripheral localization pattern, approximately 10% of the cells contained a short fluorescent polar arc ("A" in Fig.2a). The polar arcs were usually present at only one of the two cell poles.
Effect of MinE on the Gfp-MinD distribution pattern: polar zones.Evidence that MinE can induce changes in the distribution pattern of membrane-associated MinD came from experiments in whichgfp::minD was coexpressed withminE in a Δmin strain (RC1/pSLR22/pDB188 [Δmin/Para-gfp::minD/Plac-minE]) by growth in the presence of 0.001 to 0.005% arabinose. Under these conditions many cells in the population contained a long fluorescent zone at one end of the cell (Fig. 3). In unfixed cells, the polar zones of Gfp-MinD oscillated from pole-to-pole (Fig. 4) as has previously been described (16).
Quantitative Western blots, made by using anti-MinD antibody, were done to exclude the possibility that the redistribution of Gfp-MinD might have reflected secondary increases in Gfp-MinD concentration rather than a positive effect of MinE on MinD distribution. This showed no significant difference in the concentration of immunoreactive Gfp-MinD between cells that did not express MinE and those that coexpressed MinE and Gfp-MinD (data not shown). This excludes the possibility that the effect of MinE was due to a secondary change in MinD concentration.
Effect of MinE domains on localization of Gfp-MinD.Previous work has indicated that the topological specificity domain of MinE is located within the C-terminal region (MinE36–88) of the 88-amino-acid MinE protein and that the anti-MinCD domain that is capable of suppressing the action of the MinCD division inhibitor is located in the N-terminal region of the protein (MinE1–22or MinE1–34) (13, 20). It has been suggested that the topological specificity domain interacts with a topological target at midcell to direct MinE localization at midcell, whereas the anti-MinCD domain of MinE is thought to interact with the MinCD system via MinD (17).
We therefore asked whether the ability of MinE to cause Gfp-MinD to coalesce into an extended membrane-associated structure at the cell pole required both of the MinE domains. In these experimentsgfp::minD was expressed in a Δmin host from pSLR22 (Para-gfp::minD) and C-terminal or N-terminal MinE fragments were expressed underPlac control.
Coexpression of Gfp-MinD with a MinE fragment that contained the topological specificity domain but lacked the anti-MinCD domain (fragment MinE22–88, in pSY1057) did not significantly alter the pattern that was present in the absence of MinE (Fig.5c). Fluorescence was predominantly peripheral along the length of the cell, and no localized fluorescent zones were observed. Western blots with antibody directed against the C-terminal region of MinE showed that the concentration of MinE22–88 was severalfold higher than the concentration of full-length MinE (MinE1–88) in the experiments in whichPlac-minE1–88 was coexpressed withgfp::minD (data not shown). Therefore, the failure of the C-terminal MinE domain to affect the Gfp-MinD pattern was not due to a lower cellular concentration of the fragment compared with the concentration of MinE1–88 in the parallel experiments.
In contrast to the failure of the C-terminal MinE fragment to change the Gfp-MinD distribution pattern, N-terminal fragments MinE1–32 and MinE1–53, which contain the anti-MinCD domain but lack the topological specificity domain, did significantly alter the distribution pattern of Gfp-MinD. In these cases, instead of the pattern of peripheral fluorescence that was characteristic of cells that expressedgfp::minD in the absence of MinE, cells that coexpressed Gfp-MinD with MinE1–32 or MinE1–53 contained long fluorescent zones at the cell pole (Fig. 5a and b). These were present in most cells in the population and were similar in appearance to the polar zones in cells that coexpressedgfp::minD and full-lengthminE (Fig. 3). The pattern was the same when expression of the N-terminal MinE fragments was varied over a wide range by growth at IPTG concentrations ranging from 0 to 2 mM.
The pattern was the same in fixed and unfixed cells (Fig. 5a and d), indicating the polar zones of fluorescence were not fixation artifacts and were not artifacts induced by UV irradiation during examination or by the attachment of unfixed cells to the glass slide. In cells of normal length (≤5.0-μm cell length), the zones were always located at one end of the cell. In some longer cells, fluorescent zones were present at both poles and were sometimes also present elsewhere along the length of the cell. The polar fluorescence was predominantly peripheral, indicating that it represented membrane-associated Gfp-MinD. Strikingly, whenever polar zones were present, the remainder of the cell periphery was essentially nonfluorescent (Fig. 5a, b, and d). This was in sharp contrast to cells that expressed Gfp-MinD in the absence of MinE, where the fluorescence was distributed around the entire cell periphery. This implies that the MinE fragments were responsible for the recruitment of essentially all of the membrane-associated Gfp-MinD into the polar zones.
Studies of unfixed cells showed that the N-terminal portion of MinE induced both the segregation of Gfp-MinD to one pole and its subsequent back-and-forth movement to the opposite pole (Fig.6). The relatively slow oscillation may reflect lower-than-optimal ratios of MinE to MinD, which can significantly affect the rate of oscillation (16). The presence of oscillatory pole-to-pole movement of Gfp-MinD in the presence of MinE1–53 indicates that the mechanisms for the MinE-dependent polar localization and for transpolar movement of MinD do not require the topological specificity domain of MinE.
Localization of MinE-Gfp and MinE1–53-Gfp in the presence of MinD.Full-length MinE (as MinE-Gfp) forms a ring at midcell when expressed in the presence of MinD (14). This led to the suggestion that the midcell MinE ring might be responsible for sequestering Gfp-MinD to one of the ends of the cell to form the polar MinD zones and might also play a role in inducing disassembly of Gfp-MinD from the polar membrane binding site and subsequent pole-to-pole movement (16).
It has been previously shown that MinE1–33-Gfp fails to form midcell MinE rings (14) although, as shown in the present work, MinE1–32 was capable of inducing formation of polar zones of MinD-Gfp. Because MinE1–53 also induced the formation of polar MinD zones, we used MinE1–53-Gfp to determine whether MinE1–53 was capable of forming a MinE ring at midcell. Localization studies in cells where MinE1–53-Gfp was coexpressed with MinD failed to show the characteristic MinE rings that are seen with full-length MinE-Gfp (Fig.7). This confirms that the N-terminal MinE domain is unable to localize at midcell in the absence of the C-terminal topological specificity domain, although it is capable of inducing the redistribution of MinD into polar zones. These results suggest that a MinE ring is not required for the formation of polar zones of MinD.
It has not been directly shown that MinE-Gfp, and MinE1–33-Gfp and MinE1–53-Gfp, behave similarly to the non-Gfp proteins in the ability to induce formation of polar MinD zones. However, wild-type MinE-Gfp can restore a wild-type phenotype to MinE-deficient cells (reference14 and unpublished results). Similarly, MinE1–53-Gfp behaved like underivatized MinE1–53 (20) in its ability to induce minicell formation in wild-type cells (Fig. 1h, i), presumably by interacting with MinD. These observations suggest that the presence of the Gfp components does not significantly interfere with function of full-length MinE or the N-terminal MinE domain.
Proper placement of the E. coli division septum requires that MinD and MinE function cooperatively to modulate the division potential of cellular sites that are located at midcell and at the cell poles. A MinD-MinE interaction in this process is implied by the fact that localization of MinE at midcell requires MinD, that MinD is required to make the MinC division inhibitor sensitive to suppression by MinE, and that MinE is required for the formation of MinD zones at the cell pole.
Gfp-MinD is capable of associating with the membrane around the entire periphery of the cell in the absence of MinE and MinC, as shown by Raskin and de Boer (16) and as confirmed in the present study. In contrast, the membrane association of MinE (14) and MinC (9, 15) both require the presence of MinD. These observations suggest that the membrane attachment of MinD is the initial step in the membrane assembly of the Min proteins. The MinD sequence does not include an apparent membrane-spanning domain, and cell fractionation and immunoelectronmicroscopic studies suggest that MinD is a peripheral membrane protein (2). This suggests that MinD is likely to interact with another membrane component that anchors it to the membrane surface.
MinE dramatically changes the membrane distribution of MinD so that essentially all of the membrane-associated Gfp-MinD is recruited into a broad zone at one cell pole (reference 16 and this study). Previous studies with Gfp-MinE (14) have shown that MinE forms a ring near midcell under the same conditions that lead to formation of the polar zones of MinD, raising the possibility (16) that the midcell MinE ring plays a role in the observed redistribution of membrane-associated MinD. The present observations suggest that the two events, i.e., the formation of the midcell MinE ring and the formation of polar zones of MinD, are unrelated phenomena. Thus, in the present study the N-terminal domain of MinE, which did not form a midcell MinE ring in studies of MinE1–53-Gfp (this study) and MinE1–33-Gfp (14), was capable of inducing formation of polar zones of Gfp-MinD with high efficiency. This argues against models in which the MinE ring at midcell acts as a gasket to sequester Gfp-MinD to one end of the cell and/or to provoke release of Gfp-MinD from one pole so that it can move to the opposite pole (16).
Because MinE1–53 and MinE1–34 fragments retain their ability to counteract the division-inhibitory action of MinCD in a MinD-dependent fashion (13, 20), it is likely that the N-terminal MinE domain is the domain that interacts with MinD. It is this interaction that presumably provokes the redistribution of membrane-associated MinD to the cell pole.
We suggest the following sequence of events to explain the cooperative actions of MinE and MinD, based on the idea that formation of the MinE ring at midcell and formation of the MinD zone at the cell pole both result from the lateral movement of MinD within the two-dimensional membrane matrix. First, MinD associates with the inner surface of the cytoplasmic membrane around the entire periphery of the cell. Second, the N-terminal domain of MinE interacts with the membrane-associated MinD. This recruits MinE to the membrane. We speculate that the MinD-MinE interaction may alter MinD or its membrane attachment to permit MinD molecules to diffuse laterally within the two-dimensional membrane matrix, possibly in association with its putative membrane anchor. Alternatively, MinD may always be laterally mobile within the membrane. In this case, MinE could modify MinD to increase its affinity for polar sites (discussed below). This alternative is perhaps less likely since the fact that Gfp-MinD forms polar arcs in the absence of MinE (Fig. 2a) implies that MinD has affinity for the cell pole independently of MinE. In either case, the laterally mobile MinD molecules are suggested to be responsible both for the formation of the MinE ring at midcell and for the formation of the MinD polar zones. Third, when the laterally mobile MinD-MinE complex encounters the putative topological target for MinE at midcell, the midcell target interacts with the C-terminal topological specificity domain of MinE, thereby anchoring MinE as a ring structure at midcell and releasing it from its MinD carrier. This finding is consistent with the observation that the topological specificity domain is required for formation of the midcell MinE ring. Fourth, unrelated to formation of the MinE ring, the collision of laterally mobile MinD molecules with a hypothetical membrane-associated nucleation site adjacent to a cell pole leads to formation of a side-by-side array of MinD molecules (the polar zone) whose assembly depends on collisional interactions within the membrane matrix. The two-dimensional MinD lattice would be expected to grow and coalesce until most or all of the mobile membrane-associated MinD molecules were captured by collision with the polar lattice. This would explain the striking observation that only a single Gfp-MinD zone was present in most cells, with no visible fluorescence elsewhere in the membrane.
The fact that the MinD zone is apparently formed at only one pole might reflect a rapid MinD assembly process following the initial interaction with one of the polar nucleation sites, a process similar to the cooperative assembly process suggested by Raskin and de Boer (16). The forces that capture and retain MinD molecules within the polar zone have yet to be defined. The lattice could be based on direct interactions between MinD molecules or could involve the noncovalent cross-linking of MinD molecules or oligomers by another component that would also be part of the polar lattice structure. The suggested model invokes lateral diffusion of MinD molecules as the key event in the formation of the MinD polar zones and in the MinD-facilitated formation of the midcell MinE ring. The possibility also exists that the lateral translocation event might in part be an active process in which MinE modifies MinD into a form that can be actively translocated along the membrane.
A precedent for the capture of mobile membrane molecules into a single structure exists in the well-established ability of antibody molecules or lectins to induce the redistribution of eucaryotic membrane-associated surface proteins by noncovalently crosslinking them into "patches" and "caps" that are reminiscent of the Gfp-MinD structures described here (7, 12, 18). Ultimately, all of the proteins are captured into a single large domain, one analogous to the Gfp-MinD zones that are formed at the cell pole.
In an entirely different type of model, MinD would move directly from the cytoplasm to the polar membrane sites after its interaction with MinE. This cannot be excluded although it would require a second mechanism to explain the requirement for MinD in formation of the midcell MinE ring. Further work will be needed to distinguish between these and other possible models.
This work was supported by grants from the National Institutes of Health to L.I.R. (GM41978 and GM53276). S.L.R. was a Long Term Fellow of the Human Frontiers Science Program.
- Received 26 April 1999.
- Accepted 3 November 1999.
- Copyright © 2000 American Society for Microbiology


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I have a Bachelor of Counselling in Person-Centred Counselling (PCC) and have trained in Emotionally Focused Therapy (EFT) for Individuals, Couples and Families.
I am a member of the New Zealand Association of Counsellors (NZAC) working within their code of practice.
I am passionate about helping children, young people and adults as individuals, couples or families to live and relate well.
I have a special interest in working with couples whose relationships are distressed or who would like to deepen their relational bonds.
I operate my private practice in Rural Canterbury, in the Selwyn and Ashburton Districts. See my website for details.

subset: commoncrawl


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In the controversial TV comedy series 'Trivia' now on air, there's a fake surgeon who purports to have obtained a medical degree from an unknown university in the Philippines. But his alma mater cannot even be found on the internet nor can the city where he spent five years studying be found on the map. Last week, however, Minister of Health Hassan Hashemi at the inauguration ceremony of his new education deputy spoke of a fact which is not dissimilar to the fictional comic character in the TV series.
He spoke about students who leave the country to study abroad. A phenomenon, which he claims, is doing more harm than good. Students who spend big money to study in subpar universities in countries such as UAE, Malaysia, Turkey, the Philippines, etc are seemingly indifferent to the vast education resources in the country, he says. According to Hashemi -who is an accomplished ophthalmologist, ''the trouble begins when these graduates return home to practice their craft.''
In for Disappointment
The stampede over travelling overseas for higher education instead of studying at home began several years ago, but moved into unprecedented territory in the recent past. Even historic gains in the greenback and other foreign currencies against the Iranian rail failed to slow the process. With the gradual return of these graduates, their expectations that their degrees be endorsed by the ministry of higher education in Tehran are likely to be frustrated.
''The assessment process for universities can vary from case to case but only the universities whose names appear on the ministry's list of approved varsities get the chance to be assessed'', says Dr. Hamid Akbari, head of the education service at the ministry of health in an interview with the Persian-language daily 'Iran'. He added that final approval of the degrees obtained overseas is subject to a series of theoretical and practical tests conducted to ascertain the applicants' competency and qualification to work in the country.
Double Attraction
Akbari says students who study in ''substandard'' universities'' do not receive support from the health ministry - including subsidized foreign currency, adding that one-third of the 14,000 medical students studying abroad are being trained in universities deemed low-grade. This number of students is based on certificates sent to his office for verification. Akbari says the annual tuition these students pay vary from $3,000 in neighboring states to a whopping 30,000 in Europe.
The high figures prompted the minister to announce some reforms to help address the wave of low-quality foreign degrees streaming into the country. . Hashemi called for the expansion of international branches of Iranian universities in other countries to attract both the domestic population wanting to study abroad as well as the Iranian expatriates. Regarding the initiative, Akbari said the ministry intends to make room for college applicants who fail to enter state and Azad universities by accepting them in international universities abroad at the students' own expenses, thereby preventing them from receiving cheap education elsewhere.
''Many of these people are interested in studying medicine, dentistry or pharmacy, but the tight competition keeps them from entering even Azad (open) universities and hence the search overseas."
The systematic increase in the value of hard currency notwithstanding, and the cost of living, figures show presently 61,000 Iranians study abroad – 26,000 PhD candidates. This is while according to the ministry of higher education, there are over 25,000 vacant seats in universities at home. According to Nesha webstie- a forum for Iranian students based abroad - these students are mostly in Malaysia, United States, Canada and Germany.
'' The problem is despite the list of approved universities on our website, we still see people fall prey to misinformation and present the ministry with certificates we cannot approve'', says Mohammad Mahdavi, director of the international education office at the ministry of higher education. Iran's cultural attaches are there to offer counseling on the validity of universities which he said are ranked on a scale from "poor to excellent."


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Basiji thugs, and Lebanese Hezbollah thugs are the most notorious Islamists in Iran. But why? Iran's government says the Basij count some five million members. Independent analysts put the number closer to one million, out of an Iranian population of about 75 million. The Basij don't wear uniforms. Men typically sport beards, and often wear loose-fitting shirts that fall untucked over their pants. Women members are usually covered in head-to-toe black chadors. Rank-and-file members don't draw permanent salaries, and just receive high wage for the temporary mercenary job in fighting against the people and the people's will. They enjoy special consideration when competing for university admission or government jobs. A Basij chapter operates out of every officially sanctioned institution, private or government owned. Ministries, universities, factories, schools, mosques and hospitals all house Basij units. Joining the Basij can be as easy as signing up. But members are carefully vetted. Indoctrination includes theology and ideology seminars, then military training. Under AN, authorities reinstituted street checkpoints, manned by Basij and separate morality police, who monitored everything from men's haircuts to how women wear their mandatory headscarves
In 2005, Basij forces were placed under the direct command of the Sepah (IRGC or Iran Revolutionary Guard Corps). The Sepah, with responsibility for internal security, runs a sort of parallel military, with its own air force and naval branches, its own ministry and extensive business activities. The Sepahi and Basiji thugs say: " Our society is now at the verge of sin and filled with antirevolutionary people … The Satellite TV channels corrupt the people … now the people want freedom and democracy, not Islam … They are brainwashed and become anti-Islam and antirevolutionary … They don't want to obey God's order, they want to obey their own will and their own orders … It's a sin, a great sin … It is now everyone's Islamic and revolutionary duty to crush these antirevolutionary forces … The people must obey God, and it's not a selection, it's a duty, a religious duty … the people could not do what they want to do, we f-u-c-k them all, it's a God's order and our dear leader's order that has connection with God and the Mahdi " Basiji thugs fought against I-s-r-a-e-l in Lebanon in the 1980s and helped train the armed militia of Hezbollah, the Lebanese Shiite group. In fact, the Sepah (IRGC), created and trained the Hezbollah in Lebanon, and they are the main allied Muslim fanatics.
No Gaza – No Lebanon
In the recent years, one of the main chant of Iranians is: " No Gaza, No Lebanon — I will die just for Iran " but why do Iranian say that? On the one hand, In the last 32 years the Islamic regime has supported the Hamas, Hizbullah and other Islamic groups in the ME. But Iranians don't like this kind of unconditional support. Indeed, they have tired of Islamists and plundering of the oil money and financial support of Hezbollah or Hamas. On the other hand, Basij and Sepah kill, torture, rape, and beat Iranians, and Hamas and Hezbollah militia directly support them. Al-ShargholOsat Arabic newspaper said: Lebanon's Hezbollah at least sent 1500 members of its militia to Tehran to help Basiji Thugs. In fact, we, i.e. all people that live inside Iran, can see many Hezbollah militia in Tehran that kill, torture, and beat Iranian pro-democracy protesters in the streets. The Left demonstrated in the cities of the EU and the US for Hamas and Hezbollah. The left protects, encourages, demonstrates, for rotten regimes. But they don't demonstrate for Iranian protesters, for millions of secular and pro-democracy protesters in Iran, and for condemning Basij and Hezbollah militia, who kill, torture, rape and beat Iranians in the streets and jails. Shame on them. Shame on the lunatic left.


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No. 14 ASU women hold No. 9 Stanford to all-time scoring low
It's not shocking that No. 14 Arizona State women's basketball beat No. 9 Stanford again on Monday night.
But to hold the historic powerhouse Cardinal to a school record low 31 points at Wells Fargo Arena is beyond what even ASU could have expected from its suffocating man defense.
The Sun Devils never trailed and led by as many as 20 points in a 49-31 win, becoming the first Pac-12 team to beat Stanford in three straight regular-season games since 1988. The Cardinal previous scoring low was 32 vs. Missouri in 1984.
ASU beat a top-10 team for the second time this season, previously downing then-No. 10 Florida State 68-56 on Dec. 21, and now are on an eight-game win streak.
"If we get our offense going like our defense, look out," ASU coach Charli Turner Thorne said. "I just thought we had a tremendous effort, physically, mentally, emotionally – just really worked hard the entire game and didn't let things bother us even when our offense wasn't going. We just got back, dug in, worked hard and never let them get comfortable and in any offensive flow. In terms of having a great team defensive effort, it was fantastic."
No. 17 ASU women's baketball hosts No. 11 Stanford
No Stanford player scored more than seven points and the Cardinal (11-3, 1-1 Pac-12) shot 25.6 percent.
ASU (11-3, 2-0) led 41-32 in rebounding thanks to junior forward Sophie Brunner with 10 boards and 12 points. Guard Arnecia Hawkins also scored a dozen, although on 5-of-20 shooting. Point guard Elisha Davis added nine points, six rebounds and three assists.
"It was whoever was going to hit first was going to get the rebounds, and tonight we really took that to heart," Brunner said. "I definitely think we were the more aggressive team. When you're the more aggressive team, it's a different type of feel. You have that mind-set you're going to get every ball, get every rebound, every loose ball. You're going to be up in their face pressuring them. If you don't get the ball, it's kind of like why don't I have the ball?"
Stanford had two long first-half scoring droughts and shot just 23.8 percent (5-of-21) as ASU built a 26-13 lead. "I couldn't believe the halftime score," Turner Thorne said.
The Cardinal went scoreless for 6:26 of the first quarter, falling behind 14-4, before a Karlie Samuelson 3-pointer from the corner. In the second quarter, ASU held Stanford scoreless for 4:42, increasing its lead to 26-9 before the Cardinal scored the final two baskets of the half.
ASU also dominated the first half, leading by as many as 20 points, in a win over No. 21 California on Saturday.
Stanford trailed 31-19 halfway through the third quarter when Hawkins and Davis hit 3-pointers in an 8-0 ASU run that largely put the game away. The Cardinal got no closer than 13 (39-26) after that.
"We are getting a little more poised and smarter playing with a lead," Turner Thorne said. "Early on, we weren't doing a good job with that. We had a really tough preseason and we've been through a lot of situations. We've come from behind and had back and forth games, and this team has really grown with that."
ASU shot just 30.9 percent and was outscored 20-12 in the paint but had a 12-5 edge in points off turnovers and 16-9 on second-chance opportunities.
"Our coaches gave us beautiful scout that allowed us to know the personnel inside and out," Davis said. "All that goes to them that allowed us to played the defense we played to hold them those few points."
"That'll be something fun to reflect on" after the season, Turner Thorne said of holding her alma mater, a two-time NCAA champion with 11 Final Four appearances, to an all-time scoring low. "Right now we're just going to keep grinding. We've got a lot of basketball left and this team is showing it can have a good year."
ASU is at Washington (11-3, 2-1) on Friday.
AP top 25
1. Connecticut (32 first-place votes) 800 points
2. South Carolina 765
3. Notre Dame 735
4. Texas 705
5. Ohio State 630
6. Baylor 627
7. Mississippi State 616
8. Maryland 580
9. Stanford 521
10. Kentucky 502
11. Oregon State 495
12. Tennessee 460
13. Texas A&M 416
14. Arizona State 356
16. Northwestern 235
17. Oklahoma 229
18. Duke 215
19. Florida State 202
20. Missouri 198
21. California 183
22. South Florida 168
23. Michigan State 109
24. DePaul 94
25. Seton Hall 78
Others receiving votes: Syracuse 52, Virginia Tech 45, Miami 43, Iowa 20, Oklahoma State 14, Georgia 12, Oregon 11, USC 9, TCU 5, Louisville 4, South Dakota State 4, UTEP 4, Florida 3, Iowa State 3, Duquesne 2, Green Bay 2, Purdue 2, Rutgers 2, Washington 1.
My AP vote
1. Connecticut
2. South Carolina
3. Notre Dame
4. Maryland
5. Texas
6. Baylor
7. Ohio State
8. Stanford
9. Kentucky
10. Tennessee
11. Oregon State
12. Arizona State
13. Mississippi State
14. Texas A&M
16. Missouri
17. Michigan State
18. California
19. Florida State
20. Oklahoma
21. South Florida
22. Duke
23. Georgia
25. Syracuse


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Good thing, too. Loving the conditions and absolutely blowing out their competition was the J/111 SYMMETRY, taking 1st in PHRF D Class and 1st Overall! Congratulations to Howard Turner and his crew on SYMMETRY of Jay Crum, Joe Crum, Paul Stone, Michael Johnaon, Keith Stahnke from Santa Cruz YC!
Also, sailing an awesome race was the J/88 BLUE FLASH, taking a fourth in PHRF F Class- Scott Grealish and crew of David Aymar, Kerry Poe, Andrew Haliburton, and Michael Haliburton from Willamette Sailing Club in Portland, Oregon. Sailing photo credits- Sharon Green / UltimateSailing.com. For more Coastal Cup sailing information


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Modern businesses are able to locate their ideal staff with pinpoint precision, largely down to the technology and techniques available to them. Increasingly innovative search methods and new software allows employers to scout out prospective employees on a narrow set of criteria, and still find the person for the role.
If you're looking to further your career, you could be doing yourself a huge favor by expanding your skillset and fine-tuning your résumé to make yourself attractive to modern employers. While preparing for tricky interviews and getting the job is a matter of practice and quick thinking, these skills will get you into that interview room in the first place.
Demonstrating Your Specialization
Many businesses – and especially smaller ones – are run by jack-of-all-trades who are talented in having a go at every aspect of the business. However, increasingly, as Global Resources, LLC suggested in July 2017, small businesses are taking advantage of specialized professionals to gather bespoke advice. This is largely due to the way the internet has made it easy for professionals of all kinds to find business and build their reputation, independent of a host service.
To take advantage of this, make sure that your online presence and résumé reflect your specialization. Make a conscious effort to keep your skills up-to-date and well-trained. If you already work for a business as a specialist, you can benefit yourself and your company by requesting time or money for fresh training.
Critical Thinking and Problem Solving
More than ever, employers are rating critical thinking as one of the very top skills sought in their prospective hires. Critical thinking is the hallmark of universities, usually, and you don't see it focused on in the workplace. Especially not in vocational workplaces. However, technology is shaping every workplace like never before, with disruptive technology reducing the headcounts for many companies and transforming ways of working. Being able to demonstrate a commitment to critical thinking, through techniques such as continuous improvement, will demonstrate your adaptability to your employer.
Coming hand in hand with critical thinking is problem solving. The same ideas for the value of problem solving come into play here, just on a shorter term basis.
So called 'soft skills', like communication, organization and teamwork, are at the core of every business. However, there are a shortage of workers with soft skills. They are often seen as the flipside to the hard skills – like critical thinking – gained through education.
In order to get yourself seen by prospective employers and create your own personal portfolio of skills, you must develop your soft-skills. Communication can be simple; make sure you're well versed in how to address people from a range of angles, and are able to clearly articulate your message in simple, plain writing. There are now plenty of apps for communication skills at hand with your smartphone or other device to help you with this.
Organization can be expressed through your online presence and resume – is it well organized? Is it fully up to date? Teamwork, of course, can only be built with other people. You might find it worthwhile to suggest team-building exercises with your employer if you feel lacking, and put these onto your resume.
Modern employers have the skills to pluck the finest candidates out of the pool. For that reason, the modern candidate needs a lot – drive, specialization and all-round life skills. If you're looking to further your career, you'll give yourself a big boost by paying attention to these tips.


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- Fonds
- 1877
The fonds consists of McLean's survey book for a survey near Edmonton.
McLean, A.I.
The fonds consists of McLean's survey book for a survey near Edmonton.
McLean, A.I.
The fonds consists of photographs depicting the construction of the Canadian Pacific Railway, Pacific Section, including views of landscapes, tunnels, structures, and portraits of the Onderdonk family, business associates, and friends.
Onderdonk, Andrew J.
The fonds consists of Green's diaries relating to survey work for the Canadian Pacific Railway and a survey of Saltspring Island.
Green, Ashdown
C.F. Hanington fonds : 1874-1876
The fonds consists of Hanington's letterbook.
Hanington, C.F.
The fonds consists of a diary of Canadian Pacific Railway surveys of Port Moody and Fraser Valley. [Also available on microfilm.]
Gamsby, C.H.
The fonds consists of journals describing Daniel Mainguy's travels, his life at Chemainus and his work on the Canadian Pacific Railway. [Also available on microfilm.]
Mainguy, Daniel Wishart
The fonds consists of a diary (1897) kept by Duchesnay while examining the Stikine River and the country between Telegraph Creek and Teslin Lake for the proposed Canadian-Yukon railway.
Duchesnay, Edmund, d. 1901
The fonds consists of albumen prints of the CPR line from Port Arthur to Victoria.
Deville, Edouard
The fonds consists of copies of outward telegrams of George A. Keefer pertaining to progress reports on railway construction.
Keefer, George A.
The fonds consists of George Hargreaves' diary, survey notes relating to work for the Canadian Pacific Railway, and a "sketch" sent to friends in England.
Hargreaves, George, d. 1910


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- This event has passed.
Vásquez-Levy featured as Theologian in Residence, Dialogues with Iowa AG
March 1, 2019 @ 7:00 pm - March 3, 2019 @ 12:00 pm
PSR President Rev. Dr. David Vásquez-Levy has been selected as the featured theologian in residence at Ames United Church of Christ's 35th Annual Theologian in Residence Weekend. The theme of the event is "Immigration Matters: Joining Together, Finding Solutions" and invites attendees into a new conversation about immigration that examines the long-range consequences of militant Immigration and Customs Enforcement (ICE). The event also features immigration lawyer Sonia Parras Konrad, organizer Erica Johnson, and filmmaker Luis Argueta.
On Friday, David will engage with Iowa Attorney General Tom Miller in a conversation titled "Law and Story: Reframing the National Conversation About Immigration." He will also be participating in a conversation with Argueta and others involved in the response to the ICE raid in Postville and preaching at Ames UCC on Sunday following a moderated panel discussion.Read more about this event here.


text: Alice Haine Personal Finance Editor Abu Dhabi As the personal finance editor of The National, Alice oversees the money content in the business section, from the latest investment trends to how to save, spend and invest your income wisely. Alice has been a journalist for over two decades, specialising in personal finance for the last 10 years in the UAE and joining The National in 2011. Alice started her career in the UK before enjoying stints as the editor of the weekend editions of Emirates Business 24/7 and the assistant editor of Emirates Today. Follow


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Amaysim is expanding its range of no-contract phone plan options, adding a "middle ground" $19.90 per month option to its existing pay as you go and $39.90 a month unlimited plans Here's how it works and what you need to know.
Like Amaysim's other plans, the $19.90 plan runs on Optus' network. You don't have to sign up for a contract, so you aren't tied in for more than 30 days.
The plan includes 500MB of data (and unlimited browsing on Twitter, Facebook, Myspace and Foursquare, like Amaysim's other plans). Call rates for the plan are 9 cents per minute and 9 cents for a text, which is lower than the rate on Amaysim's as-you-go plan (which has charged 12 cents a minute since May). Data above the 500MB allocation is charged at 5 cents per megabyte (or you can buy a 1GB data pack for $9.90.) If you use your $19.90, you can top up with additional prepaid credit (or postpaid charges if you sign up with a credit card) — but you still get the 9 cents per minute rate rather than the higher as-you-go rate.
In practical terms, $19.90 works out to 220 minutes of calls, which will be more than ample for many people. Overall, this sounds like a good deal. Indeed, if I was on the Unlimited plan, I'd be tempted to drop back to the $19.90 version and see if I was actually making the right volume of calls (since you can always switch back if it doesn't work). Equally, if you're spending $15 to $20 on prepaid each month, the lower call rate and extra data would be appealing. What do you think?


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Window Cornice Shelf
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d-Infinity Plays 'Ragnarok: The Great Winter" (Episode 7)
Thursday, May 9, 2019 - 8:00pm
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Assembling Cardstock Miniatures
In the Footsteps of Hercules: Venture to the Spring of Amymone (D&D 5E Actual Play)
In the Footsteps of Hercules: At the Baths of Nemea (D&D 5E Actual Play)
d-Infinity Plays 'In the Footsteps of Hercules' (D&D 5E)
Drawing "City Builder" KS Backer Monument
The new thegns of Arnborg: Svava, Gyda, and Steinhard, have traveled with their Jarl and others to the Eolhwood, in hope of returning the Rimecold Heart to the Eolhqueen of the Huldrfolk who live there, and lifting the curse that she set upon the Jarl and his people.
When the travelers arrive, they do not get the greeting they expect. The Huldrqueen accepts the Heart, and agrees to lift the curse. But the Jarl's offer of support and sacrifice to the Eolhwood, as the people of Hasafel did in the past, is met with suspicion – and the withdrawal of the Huldrfolk to the confines of their forbidding forest.
Under cover of darkness, the Eolhqueen returns, moving unseen through to the ensorcelled Arnborg camp, to question Svava, Gyda and Steinhard, individually. Impressed by what she learns, the Eolhqueen offers alliance, information and even the possibility of instruction, if they can aid her people in rekindling the frozen Womb of Jord, an ancient well sacred to their goddess.
After descending the icy cleft in the center of the well, they heroes found themselves atop a massive spire of ice, surrounded by wind and cloud unlike anything they expected to find below the surface of Midgard. Descending the spire, they found a large chamber with a rune-carved shard of ice, and defended by elemental beings of ice, with terrible claws.
After a tough fight in which some of our heroes took wounds. They now stand, amid the chamber of the ice shard, the shattered and melted remains of the ice creatures lying all around them …
View the discussion thread.


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Definitionditz / ditzy , vapid, flighty; frivolous.
Quote: Boxcover of Bullets of Broadway (1995): ' A wacky cast of characters, including a gangster's ditzy girlfriend, sexy Jennifer Tilly...'
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Podcast Description Edit
One year ago, Garrett Vandenburg became a treasured member of our team. His first task was to write a Ceiling Fan Halloween/Harvest special. After reviewing it, some thought it was too "halloweeny," so we scratched that and wrote a new one. Here it is.
Appearances Edit
|Ethan Daniels
|Kevin McCreary
|Garrett Vandenberg
|Phil Jinkus
|Mark Jones
|Mrs. Daniels
|Season 3
| 33·34·32·35·36·36.25·36.5·37·38·38.5·39·40·41·42p1·42p2·CA4·HS2·TS4·XMAS4
Key: TS = Thanksgiving Special, CA = Contest Announcement, HS = Halloween Special, XMAS = Christmas Special
Community content is available under CC-BY-SA unless otherwise noted.


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Humanities Blog: Nov. 6 ~ Nov. 10
Social Studies homework assignment: assigned on Fri. Nov. 10. Due: Monday Nov. 13.
In Social Studies this week, students completed their infographic assignments and we began learning about the fossil heritage of Alberta. Students discovered that the badlands of Alberta are a place where a great variety of dinosaur species have been found. Fossils are the remains or impressions of prehistoric organisms preserved in rock. Students viewed a powerpoint presentation made by Mr. Brewer on this topic. Paleontologists have discovered the presence of dinosaurs here in Alberta. Particular features of Alberta's landscape make it an amazing place for finding fossil remains such as the Albertosaurus, a prehistoric creature that students are reading about over the weekend for their homework assignment. Many students were fascinated by the question of how dinosaurs became extinct. A popular theory is that the extinction was caused by a large meteorite from outer space impacting the earth. While it was explained in class that the size of an object that could have led to a mass extinction was huge, we did look at a meteorite impact site in Canada as a means of comparison:
The picture above shows the Manicouagan Resevoir in Quebec. The shape of this lake is circular and it is thought to be the result of the impact of a meteor of 5 km in diameter. This weekend an article was published on the National Geographic website that speculates about the impact of the object from space that it is thought to have led to the mass extinction of dinosaurs: news.nationalgeographic.com/2017/11/dinosaurs-extinction-asteroid-chicxulub-soot-earth-science/?utm_source=Facebook&utm_medium=Social&utm_content=link_fb20171109news-dinoasteroid&utm_campaign=Content&sf157171398=1
Also this week students attended the Nose Creek School Remembrance Day assembly. Ms. Ross is to be thanked for her vital role in organizing this assembly. It was clear that students took seriously their obligation to reflect on the difficulties and dangers faced by those who undertook going into battle. They were solemn during the songs and performances that took place in the assembly. Many students in both 4E and 4F were directly involved as members of the grade 4 choir and are to be commended on the quality of their performance. All staff, students and visitors to Nose Creek were reminded of the ultimate sacrifice of our war dead who paid the ultimate price to ensure our freedoms.
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June 2018


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It's my birthday tomorrow and a new batch of cakes is ready just in time for it.
The photos are terrible, as I need to take them in daylight, but I was so happy to have my own little batches of 'Happy's to share my Birthday with, I needed to post them now.
Better photos and some more info will follow soon, I promise.
Have a fantastic March 20th!!
***Virtual Birthday Cake for all***


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Losing Our Forty-First President
With the recent passing of George H.W. Bush on November 30, 2018, the United States lost its forty-first president. Not only was Bush an excellent countryman, but his professional career and achievements also rival those of legend. At the ripe old age of 94, Bush passed shortly after his wife, Barbara Bush, who also passed in 2018. Both of his children have also followed in his footsteps, with George and Jeb Bush both running for president and the former serving two terms shortly after his father.
George H.W. Bush's funeral was elaborate and staged in three parts. Although much of the fanfare surrounding many previous presidents' deaths was absent, including the traditional performance of "Hail to the Chief," Bush's funeral was still a spectacle to behold. Leaving behind meticulous instructions for his state funeral, the first stage was comprised of an aerial flyover by the United States Air Force in Missing Man formation. His body was then lifted in by air and carried to the George Bush Presidential Library in College Station, Texas.
Stage two consisted of Bush's remains traveling to Washington D.C. where he was given a 21 gun salute and the United States Air Force Band performed "My Country, 'Tis of Thee." His body remained in the Capitol Hill rotunda from December 3 to the morning of December 5. It was here that numerous tributes were given and many from across the country traveled to the nation's capital to pay their respects. Finally, the last stage occurred in Bush's home state of Texas where the church service and his final burial were the main events.
Beyond the physical funeral, the funeral served to unify both the Republican party and the nation as a whole, even if for a brief period. Important dignitaries that attended included current president Donald Trump as well as former presidents Jimmy Carter, Bill Clinton, George W. Bush, and Barack Obama. Their wives also attended with them being influential figures in their own right. The emotional eulogy given by Bush's son, George W. Bush, reached YouTube's number one trending spot and touched the hearts of millions. Not only was the former president speaking for the nation, but also as a son grieving for his father. The splintered Republican party came together to mourn the death of their fallen leader and were able to get over their differences for the time being. It truly was a spectacle to behold.
Laurence Yang is currently a senior at Plymouth High School. He is a varsity swimmer, and his favorite sports to watch are basketball, football, and soccer....


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The Paradox of Silos
In my consulting work the word silo has begun to show itself everywhere. Some wax lyrically about the successes of specialization brought about by silos, whilst others complain about the breakdown in communication that has resulted from more and more independent silos. Having completed my graduate training at a medical school, and then working in the hospital system for some time, I witnessed the successes and failures of increased silo development in medicine.
Doctors, nurses and other medical professionals seldom collaborated as equal contributors in patient care. Doctors split themselves into surgeons and the internal medicine specialists. This split represents much more than what each specialist does and creates an unhelpful hierarchy. On the other hand, super-specialization has increased the quality of those medical disciplines and thus saved lives. This situation is not uncommon in many professions and organizations.
This paper is an attempt to understand silos as a human phenomenon and to locate them in an evolutionary context. I will also attempt to look at the impact silos have within a developmental model and to see whether there is a possibility to hold on to the positives they bring whilst minimizing their pitfalls.
It appears from looking at our history as a species that silos are an innate part of our development, and our success as a species.
Current anthropological theory posits that homo sapiens' success in colonizing the planet is due to the combination of two major factors. The first is our unique ability to collaborate and cooperate in large groups. What is needed to drive collaboration is a common belief and a common foe. Other species do collaborate, but not in large groups like sapiens. Imagine trying to coordinate a few thousand chimps in a stadium.
The second reason for our success is related to our competitive spirit. Homo sapiens appear to have an inbuilt drive to divide the world into 'us' and 'them'. We find ourselves in a constant competition with the 'other'. The combination of competitive spirit and the capacity to collaborate is theorized to have developed as a function to protect valuable resources such as food and fuel.
Put together, these two factors have resulted in homo sapiens becoming the most formidable species this planet has ever seen. When we collaborate and compete we are able to undertake both amazing feats, such as putting a person on the moon, and acts of atrocity such as the holocaust.
It is these factors that have driven the ever-increasing complexity in our work lives. From the industrial revolution onwards we have seen the division of labor and increased specialization in developing organizations. This has resulted in the creation of what we now refer to as silos.
It is the paradoxical interplay between collaboration and competition that has made these silos problematic for modern organizations. With the entrenchment of silos, competitive energy gets diverted from outside to inside the organization, to defending our resources from other departments in the same organization.
These resources include power, money and influence. The different silos compete with each other for turf and in so doing lose focus on larger organizational or societal goals.
Gillian Tett's new book, The Silo Effect, clearly articulates the role silos played in the 2008 financial crisis. She shows complex silos proliferated in financial services organizations, which developed due to competition around specialist knowledge and internal competition for rewards (bonuses). These organizations eventually imploded through internal competition, hidden information and lack of communication.
So if the development of silos is a natural feature of us as a species, and if we need competition as well as collaboration, is there any way out of this dialectic? I believe that to move out of a binary view on the subject we need to look to developmental theory.
In our maturation process we move through at least three different development phases. The first: early dependency. In this phase the child literally cannot survive without their caretakers. This dependency is not merely physical, but psychological as well. In startup organizations a similar dependency can be seen. Everybody gets involved in almost everything and all are ready and agile enough to take on the competition. Every part of the company depends on the other and interacts and communicates often.
Should the sapiens child have their dependency needs taken care of, they gradually move to a position of independence. We are all fully aware of the the adolescent who shouts out
"leave me alone I don't need you". This is the second stage: the attempt to break childlike dependencies. The adolescent hopefully individuates to become a more or less independent person.
The achievement of the individual and their importance is one of the pillars of Western democracies and capitalism. Most organizations are dominated by the idea of the individual, so it is not surprising that organizational culture tends to be strongly "I" dominated. It is due to the strong emphasis on the individual, or individual units, that I believe silos begin to form. Sales team, investment silos and operations departments compete for autonomy and the scarce resources the organization has to offer.
Children who are able to obtain a sufficient level of independence move on to the third phase of development: the stage of interdependence. Here the individual exists independently and at the same time depends on the group. It is the stage at which partnerships such as marriage becomes possible. Merely reaching adulthood does not signify moving into a phase of interdependence. Nor does the act of getting married; hence the high percentage of failed relationships in our society.
Organizations are not different. Those that are able to transition into a stage of interdependence are able to function with an ecosystems mindset. They are aware of how the independent parts contribute to achieve common goals and share a common purpose. They encourage friendly competition without it descending into outright sibling rivalry. What makes this possible? Common purpose, which is where a strong culture comes into play.
Unfortunately, our love affair with individualism means not many people or organizations ever make the shift into the interdependence phase. My work as a psychotherapist and an organizational consultant has shown me this over and over again. We tend to either remain in a state of dependence or cling to independence as though our life depends on it.
What underlies becoming stuck in independence is the fear of dependency, of losing vitality and being pulled back into a state of dependency. This fear perpetuates our belief in the individual, which reinforces the problem.
I strongly believe that the only way to really deal with the questions around silos is to help individuals and organizations discover the value of, and transition into, the space of interdependence. This change is not a simple process of behavior change, but rather a complex evolution of culture and leadership. But in many organizations, the traits that propel people into leadership and therefore drive culture can be described as narcissistic in nature. By nature, narcissism is about being stuck in the independence/dependency phase, which is all about the individual. So perhaps our true role is to help organizations out of narcissism. A rather grandiose desire in itself.
I believe we are just beginning to see the rise of organizations that are shifting into the interdependence phase. An example is Facebook, which has consciously rebelled against silo mentality. These rising giants have seen the power of collaboration and are disrupting traditional individualist business models. Can these "sharing economy" organizations help to shift us into a more interdependent space? And can they help us to solve the paradox of silos.


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Deadly Shootings & Explosions In Paris Near Charlie Hebdo Terrorist Attack: At Least 127 Killed
Parisians are horrified that there have just been multiple terrorist attacks — shootings, a hostage situation, and a series of explosions — in their country on Nov. 13. At least 127 people were killed in the attacks according to French authorities.
So scary. Many people were killed during a machine gun wielding in a Paris restaurant late Friday, Nov. 13, a new report claims. Even worse, there had also reportedly been explosions near national stadium, where the French soccer team was playing Germany. And at least 100 hostages were killed at a concert hall. The country is in disbelief. This is the deadliest violence in France in many, many years.
We can't believe what we've learned. A deadly shooting at a restaurant on the Rue Bichat, explosions near the Stade de France sports stadium (two suicide bombs were detonated) and another shooting at the Paris Bataclan concert hall, where terrorists were holding hostages, all occurred in Paris during the late hours of Nov. 13, Daily Mail claims.
Shots and screams were heard from inside the restaurant, which is super close to where the Charlie Hebdo shootings occurred in January. And at least 100 were killed in the Bataclan theater, where a hostage situation occurred, according to The Hollywood Reporter. Hostage-takers were said to be going through the venue, where a rock concert was taking place, looking for people who were hiding from them, CNN claims. At this time, the hostage-takers have been killed by police. All together, at least 153 are dead, multiple reports claim. Survivors of the attack describe the "carnage" as a chilling "bloodbath."
And it's not confirmed, but Reuters claims another shooting may have occurred at Les Halles shopping mall in Paris.
UPDATE: The French President has declared a state of emergency and closed Paris' borders.
The story is constantly developing, so keep coming back to HollywoodLife.com for all the updates. To watch live coverage of the situation, click here.
Our thoughts go out to the friends and families of the victims of this deadly attack. Celebs like Rob Lowe and Andy Cohen are also sending their prayers to Paris.
— Chris Rogers
Follow @ChrisRogers86


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Do you have "doctor phobia?"
Are you afraid of your doctor?
Are you one of those people who dreads coming face-to-face with your doctor? If so, the good news is that you're not alone—you're not even all that unusual. Many people feel nervous, impatient or scared while interacting with their doctor. The downside of this "phobia," is that it can interfere with getting the best medical care.
Some patients are intimidated by their doctors. If you are worried that you will ask a "dumb question" or give your doctor the impression that you are a "complainer," that can get in the way of staying healthy.
It's important to remember that while your doctor is a trained medical professional, he or she is a person with the same personal issues that you have. Like you, your doctor has worries, doesn't always sleep soundly, suffers from stress and has the same basic needs as you do. They may suffer from the same illnesses and discomforts many of their patients go through. Sometimes, just like you, doctors become patients.
It's so important that you and your doctor understand each other when you are talking about something as serious as an illness or symptoms of a possible illness. Communication is key to your healthcare success. By being prepared, you can make the best of the limited time you have to talk to each other.
It's your role to make sure your doctor understands your symptoms
If you are suffering from any discomfort, you need to be sure your doctor understands what you are feeling, in what part of the body you are feeling it and how often you feel it. If, instead of confronting your fear of doctors, you avoid the doctor or slough off your concerns, your health is at risk.
Be honest with your doctor[arrow_list] [list_item]To get you the best care, your doctor should know all there is to know about you, your habits, past illnesses, and your family history.[/list_item] [list_item]Don't be overly concerned that your doctor will judge you. Remember that your conversations with your doctor are privileged and confidential. Even more important, it's highly unlikely that your personal choices are unique to you alone.[/list_item] [list_item]Be prepared – It's a good idea to write down the issues you want to review with your dr before your visit. Doing so will decrease the chance that you will forget to bring these concerns to your doctor's attention.[/list_item] [/arrow_list]
- Get Ready for Public Exchange Healthcare Plans Enrollment - October 17, 2016
- Seven Pro-Tips for Family Advocates - May 6, 2016
- Beware: Price Spikes For Prescription Drugs - November 7, 2015


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my wife has the best laugh in the world. seriously, best laugh in the world. i change rooms at a party just to be closer to her when she's laughing although, i don't have to change rooms. her laugh is so big, so hearty, so wonderful in a curiously cackling sort of way that i don't have to change rooms, i just do.
not everybody likes her laugh mind you. she's been "chided" in the past for having such an inappropriate laugh in an office environment (for example). however, everytime i've heard something like this i've jumped to the rescue because i NEVER want that to die. I LOVE THIS ABOUT WENDY and don't you DARE try to squash this.
to laugh is to enjoy life and i need her to enjoy life. my heart sinks when she's struggling and it flies when she can laugh with me. my own failures don't always keep her happy but it's not like all of life is supposed to be a lark either. at any rate, i love it when she laughs.
last week i sat and listened to her talk on the phone with a very good friend. it made my day. it's not a giggle, it's a full blown, get out of your chair, what the hell was THAT sort of laugh. i LOVE it when she laughs.
hmm now i have Bruce Cockburn running through my head. Listen for the Laugh, that's good advice.
Monday, May 4, 2009
i love it when she laughs
1 comment:
- ron cole said...
Ian, the world needs more laughter. You're lucky to have that sound in your life.
- May 7, 2009 at 4:10 AM
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Reality Star Forgets Her Helmet & Driver Veers Off Overpass 01:43
Aida Nizar is known to both Italian and Spanish audiences for her time on "Big Brother." Today though, she's also known for being a little reckless on her moped. She rode her moped without a helmet and ended up crashing into a curb. Luckily, she's fine but hopefully, she'll remember a helmet in the future.
Then, it's not known why a driver in China panicked on the road, but what is known is the damage that she caused. The woman can be seen in this dashcam footage driving off the side of an overpass. Her vehicle hit the ground and spun 360 degrees before finally coming to a halt. Thankfully, she wasn't injured.


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Polaris FXR Octane Boot
WARMTH: -50 degree rating during moderate activity; multi-layer insulation provides optimum warmth and protection; removable liner with integrated support inserts.
UPPERS: Highly water-resistant upper that is stiff for increased support.
SOLES: High-traction rubber out-sole, EVA foam cushioned mid-sole.
WATER RESISTANT: Highly water resistant outsole with seam-sealed waterproof/breathable inner membrane.
ADDITIONAL FEATURES: Air cell-cushioned heel insert, upper lace eyelet holes, wrapped kick toe feature; removable liner features a double, upper and lower speedlace system for maximum support.


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Used Cars Kitchener Auto Sales
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Are you looking for a new or reliable used car in Kitchener? Finding the right pre-owned vehicle, whether it be a truck, car, SUV, or crossover, can be a fun activity.
Click to see new and used cars available in Kitchener.
There is no nicer feeling than driving away in a brand new vehicle! Whether is it is new to you or brand new off the lot,
check out your local Kitchener car dealers for both their new and used car lots.
Do you need a car loan? Will you be refinancing? Many local dealers offer auto financing at competitive rates.
Financing a new or used vehicle in Kitchener has never been easier!
What about car insurance? Protect your family and your investment with
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It is always better to be safe than sorry when it comes to adequate vehicle insurance coverage.
Check out auto manufacturers sale promotions and new car incentives as they apply to vehicle purchases in Kitchener.
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Feb 6 Opening: Outreach Pre-College Program Winter 2018 Exhibition
Tue, Feb 6, 11am - Fri, Feb 9, 2018 7pm
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Outreach Pre-College Program
Winter 2018 Exhibition: February 6th-9th
Mixed Media and Web Design
Opening Reception
Tuesday, February 6th, 6-8 PM
2nd Floor Lobby of the Foundation Building
The Outreach Pre-College Program is profoundly grateful to the Jacques and Natasha Gelman Foundation for its major support. We gratefully acknowledge our other generous donors: The Altman Foundation, The National Endowment for the Arts, and The Milton & Sally Avery Arts Foundation.
Outreach is happy to welcome back Ava's Smile for a special post-Outreach web design project with guest artist Wendy Qi.


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"Triumph or Tragedy?"
The National History Challenge is a research-based competition for students. It gives students a chance to be an historian:
More information can be found here.
The theme for 2016 is "Triumph or Tragedy?".
The video below has some information about the challenge and highlights the winner for 2015.
The History of Rock
This interactive site lets you look at the a list of the 100 top bands, with information about the artists, and traces the influence between bands.
We are learning how to ask questions and use research processes to meet and understand the challenges and opportunities ahead of us.
Not sure where to start your research? Looking for research tips and strategies to point you in the right direction?
Ask Linda.
What's Linda reading?
Linda is currently reading:
The Bass Rock by Evie Wyld


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MODERN DOG MAGAZINE has Friday Freebies and I always enter for something. I don't often win but playing is half the fun.
Last month, around Halloween they were offering Minion Halloween Costumes. One was a GIRL Minion. I must confess, a lot of my Halloween Costumes are what would be generally considered BOY costumes. And, as all my FURiends know, I am a GIRL. So that is what I told the people at Modern Dog Magazine - that if I won the GIRL costume my Mommy would HAVE to stop dressing me up as a boy.
They BOUGHT IT!!!!! I won a Minion Costume and I was so happy I danced and danced and danced. As luck would have it, "Despicable Me" was on tv and I watched it with renewed interest because NOW I would be representing GIRL MINIONS everywhere.
The costume was provided by Rubie's Pet Shop, a division of Rubie's Costumes. Take a moment to check out their costumes. They have almost anything you can imagine and for really decent prices.
Not too much later, like a couple of weeks or less, after receiving the news I had won, I received an email from Erin at Rubie's Pet Shop Boutique. She asked the important stuff like SIZE and ADDRESS. I figured I was in for a long wait.
Not so long. The costume arrived while I was at Auntie K's cozy home. The minute I saw the box, I knew what it was and I was jumping for joy!!!
I have a lot of clothes - not as many as some, but probably more than average. I wear them when the mood strikes me or when Tiffy comes over to play. It's fun.
This Minion Costume is TOP QUALITY! I loves loves loves it so much that I think I will simply wear it JUST BECAUSE! It is made of soft flannel and is sized just right for my svelte PUG body. The hat is comfortable too and I didn't try to shake it off even once!
You can't really tell from this picture but the bottom has a skirt like attachment. I almost look girly in it.
I cannot wait to SHAKE MY TAIL at the next Pugoween. I am pretty sure I will TOTALLY win the BEST BOUGHT COSTUME contest.
Tuesday, December 1, 2015
Marvelous Minion
8 comments:
- Julie said...
Noodles you look pawsome!!!!!
What a great costume, you make the bestest GIRLIE minion evers
Loves and licky kisses
Princess Leah xxx
PeeS hopes you had a great weekend
- December 1, 2015 at 10:06 AM
- Frankie Furter and Ernie said...
OMD OMD is that really YOU, Noodles??? We were SURE it was one of the Girl Minions from the Movie... visiting on your blog...
WOW it fits Pawfect and Looks Amazing on you.
Congratulations on a GREAT WIN !!!
- December 1, 2015 at 10:30 AM
- Two French Bulldogs said...
Fantastic and congratulations. That's a cool win
Lily & Edward
- December 1, 2015 at 11:27 AM
- Samantha said...
You are ADORABLE!!
- December 1, 2015 at 11:37 AM
- Idaho PugRanch said...
How cute you look Noodles!
Mr Bailey, Hazel & mabel
- December 1, 2015 at 2:48 PM
- Matilda the Boxer said...
That's a totally pawesome costume! I LOVES it!
- December 1, 2015 at 2:54 PM
- Adriana Robles said...
Vegetarian Courtesy ♥ CheesePapas
- December 1, 2015 at 5:29 PM
- Hilary said...
you look amazing!!!!
- December 3, 2015 at 4:12 AM
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Squidboards now has its own Discord server!
Welcome to SquidBoards, the largest forum dedicated to Splatoon! Over 15,000 Splatoon fans from around the world have come to discuss this fantastic game with over 150,000 posts!
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