Oligodendrocytes are one type of glial cells responsible for myelination and providing trophic supportfor axons in the central nervous system of vertebrates. Thanks to myelin, the speed of electrical-signal conductionincreases several hundred-fold because myelin serves as a kind of electrical insulator of nerve f ibers and allowsfor quick saltatory conduction of action potentials through Ranvier nodes, which are devoid of myelin. Given thatdifferentparts of the central nervous system are myelinated at different stages of development and most regionscontain both myelinated and unmyelinated axons, it is obvious that very precise mechanisms must exist to controlthe myelinationof individual axons. As they go through the stages of specif ication and differentiation – frommultipotent neuronal cells in the ventricular zone of the neural tube to mature myelinating oligodendrocytes aswell as during migration along blood vessels to their destination – cells undergo dramatic changes in the patternof gene expression. These changes require precisely spatially and temporally coordinated interactions of varioustranscription factors and epigenetic events that determine the regulatory landscape of chromatin. Chromatin remodelingsubstantially affects transcriptional activity of genes. The main component of chromatin is the nucleosome,which, in addition to the structural function, performs a regulatory one and serves as a general repressorof genes. Changes in the type, position, and local density of nucleosomes require the action of specialized ATPdependentchromatin-remodeling complexes, which use the energy of ATP hydrolysis for their activity. Mutationsin the genes encoding proteins of the remodeling complexes are often accompanied by serious disorders at earlystages of embryogenesis and are frequently identif ied in various cancers. According to the domain arrangementof the ATP-hydrolyzing subunit, most of the identif ied ATP-dependent chromatin-remodeling complexes are classified into four subfamilies: SWI/SNF, CHD, INO80/SWR, and ISWI. In this review, we discuss the roles of these subunitsof the different subfamilies at different stages of oligodendrogenesis Until recently, in the research on the workings of the brain, thecentral role in the functioning of the central nervous systemhas been assigned to neurons, and various pathological conditionshave been regarded as a result of impaired functioningof neurons. Glial cells have been assigned the function of afiller for the space among neurons, as reflected in the name:glia is translated as “glue”. Nonetheless, at present, there isno doubt about their necessity for the maintenance of axonalfunctions, for synaptic plasticity, and for the formation ofneural networks.Oligodendrocytes (OLs) are a type of glial cells responsiblefor myelination of axons in the central nervous system ofvertebrates. As a result of an extremely specialized processof intercellular interaction, each OL forms several processes,each of which repeatedly wraps a part of an axon like insulatingtape. One OL can simultaneously myelinate up to50 axonal segments . The cytoplasm isalmost absent in these processes, and, accordingly, the myelinsheath is actually many layers of the cell membrane with dielectricproperties; this arrangement prevents the scatteringof an electrical signal traveling along the axon. In addition,between the layered wrappings (sheaths) of myelin, there are~1 micron-wide gaps, called Ranvier nodes, which enablesaltatory transmission of a nerve impulse.Thus, due to the myelin sheath, the speed of the electricalsignal along the axon increases manyfold. It has beenshown that the most active axons in the brain receive heaviermyelin insulation, which allows them to work even moreefficiently. It should be noted that myelination of the centralnervous system proceeds over a long period and is the finalstage in the development of the nervous system. Accordingto magnetic resonance imaging data from humans, the bulkof myelination of most brain structures occurs in adolescenceand reaches 90 % by the age of 20–25, whereas the latematuringprefrontal cortex is the last to be myelinated . In mice, most of myelination takes place in thefirst 4–7 weeks after birth. It is worth mentioning that myelinformation continues throughout the lifespan in the form ofeither remyelination of damaged nerve fibers or myelinationof previously unmyelinated ones .Given that different parts of the central nervous system aremyelinated at different stages of development and most ofcentral nervous system regions contain both myelinated andunmyelinated axons, it is clear that very precise mechanismsmust exist to control the myelination of individual axons. Inaddition, it is becoming increasingly obvious that there is somelevel of plasticity (remodeling) based on life experience in themyelination process .Specif ication, migration, and differentiation of OLsOligodendrocytes come into being as a result of gradual differentiationof oligodendrocyte precursor cells (OPCs) thatarise during specification of multipotent neuronal progenitorcells located in the ventral zone of the neural tube. In thespecification of OPCs, one of the key factors that determinesthis localization is the sonic hedgehog (SHH) protein secretedby the cells of the notochord and floor plate. The dorsal-ventralSHH concentration gradient promotes the formation of OPCsmainly from the ventral neuroepithelium by inducing theexpression of a number of transcription factors . Oligodendrocyte precursorcells are characterized by the expression of proteoglycanNG2 and platelet growth factor receptor alpha (PDGFRα).In the absence of SHH in the anterior or spinal cord, OPCsof ventral origin do not form . After specification,OPCs proliferate and migrate along blood vessels, ensuring aneven distribution of white matter in the central nervous system. After the migrationof OPCs, some of them remain in the precursor state, whileothers – through the stage of premyelinating OLs – differentiatewithin at least 2–3 days into mature myelinating cells,which interact with axons and give rise to myelin internodes.To avoid a shortage of OLs during axon myelination, anexcess of these cells is generated, and unnecessary cells aresubsequently eliminated by apoptosis. One of the mechanismsthat determine the final OL number is competition for a limitedamount of specific growth and survival factors, suchas platelet growth factor (PDGF)-A, fibroblast growth factor(FGF)-2, insulinlike growth factor (IGF)-1, neurotrophin(NT)-3, and ciliary neurotrophic factor (CNTF) .As expected, the differentiation into OLs should be consistentwith a neuronal development program, and there areneuronal signals that control the conversion of OPCs intomyelin-forming OLs. For instance, in the peripheral nervoussystem, on the axonal membrane, there is a protein calledneuregulin 1, which controls myelination by Schwann cells;however, a similar regulatory protein triggering the myelinationby OLs in the central nervous system has not yet beenidentified. Moreover, there is evidence that there are inhibitoryneuronal signals that keep OPCs in a “suppressed” state. These inhibitory signals  coming from axons in turnactivate various regulators of transcription, such as SOX5/6,HES5, and ID2/4, which actively prevent OPCs from enteringthe stage of terminal differentiation .More and more data indicate that different areas of thecentral nervous system correspond to different OPC populationsthat are controlled by some local signaling mechanisms.Thus, in different areas of the brain and spinal cord, OPCsare under the influence of different signaling molecules. Inparticular, dissimilarities in the temporal expression of thesefactors and signals in a developing central nervous systemensure that myelination begins earlier in the spinal cord andlater in cortical regions.When going through the stages of specification, migration,proliferation, and differentiation, OLs undergo dramaticchanges in the pattern of gene expression, which require aprecisely  coordinated interactionof various transcription factors and epigenetic events thatdetermine the regulatory landscape of chromatin . Chromatin remodeling considerably affectstranscriptional activity of genes and occurs mainly due tonucleosome repositioning (under the action of ATP-dependentchromatin-remodeling complexes), chemical modifications ofhistones, DNA methylation, and interactions with noncodingRNAs .In the present review, we will examine in detail the functionsof ATP-dependent chromatin-remodeling complexes atvarious stages of oligodendrogenesis.ATP-dependent chromatin-remodeling complexesThe regulation of gene expression is possible for the most partdue to changes in the structure of chromatin: its remodeling.The main component of chromatin is the nucleosome, whichconsists of eight protein subunits (histones), wrapped by a146 bp DNA region for each nucleosome. In addition to thestructural function (there is growing evidence that it is lessimportant), the nucleosome performs a regulatory functionand serves as a general repressor of genes. It interferes withvirtually all DNA-related processes, including transcription,replication, and DNA repair . Changesin the type, position, and local density of nucleosomes requirethe action of specialized ATP-dependent chromatin-remodelingcomplexes , which use the energyof ATP hydrolysis for their functioning.All ATP-dependent chromatin-remodeling complexescontain an ATP-hydrolyzing subunit belonging to the SNF2DNA helicase/translocase family and one or more subunitsthat are bound to it . It should be notedthat these ATPases lack helicase activity for strand unwindingand therefore act only as DNA translocases  that move DNA along the surface of the nucleosomeand disrupt DNA–histone interactions. ATPases of all chromatinremodelers contain a highly conserved core ATPasedomain, which is sufficient for the catalytic activity of thecomplex; however, ATPase activity regulation is carried outby the domains flanking the ATPase domain and/or by proteinsphysically associated with it . Itmust be pointed out that tissue specificity of the subunits ofa chromatin-remodeling complex gives it unique properties,which determine its landing on tissue-specific regulatory lociof the genome .According to sequence homology of the central ATP-hydrolyzingsubunit, most of the ATP-dependent chromatinremodelingcomplexes identified so far are classified intofour subfamilies: SWI/SNF (switch/sucrose nonfermentable),CHD (chromodomain helicase DNA-binding), INO80/SWR(Inositol-requiring 80/SWi2/snf2-related 1), and ISWI subfamily(imitation switch). Aside from differences in the numberof subunits in the complex, these subfamilies are distinguishedby exclusive domains adjacent to the core ATPase region.For instance, SWI/SNF is characterized by the presence of abromodomain, CHD – by tandem chromodomains, ISWI remodelerscontain HSS helicase domains, and INO80/SWRmembers have an HSA domain (SANT helicase) .The structural differences between the subfamilies determinetheir functionality. For example, members of theSWI/SNF subfamily are mainly responsible for the removaland repositioning of nucleosomes, thereby providing access toDNA for transcription factors (in order to regulate the level ofgene expression) and for DNA repair and recombination factors.The assembly and positioning of nucleosomes is mainlyconducted by remodelers of subfamilies ISWI and CHD. Theediting of nucleosomes, namely the replacement of canonicalhistones with specialized types and vice versa, is carriedout mainly by members of the INO80 subfamily. Changingthe composition of nucleosomes allows for the creation ofspecialized regions of chromatin in a replication-independentmanner . Forexample, histone H2A.Z is a part of the nucleosomes locatedin promoter regions of most genes; the proximity of such anucleosome to a transcription start site directly correlateswith the expression level of the gene in question , H2A.X is required for the repair of double-strandbreaks .Mutations in the genes encoding subunits of ATP-dependentchromatin-remodeling complexes are often accompaniedby severe abnormalities in the early stages of embryogenesisand are frequently identified in various cancers .Remodelers’ actions during oligodendrogenesisSubfamily SWI/SNFMammalian members of SWI/SNF are large complexes of∼1.5 MDa and consist of at least 15 different subunits . They are characterized by the presence ofenzyme Brm  or Brg1  ascore translocases. These remodelers are mainly involved inthe regulation of the cell cycle and differentiation of severalcell types .A comparative analysis of genome-wide chromatin immunoprecipitation-high-throughput sequencing (ChIP-seq)data on the localization of RNA polymerase RNAPII on thegenomic DNA of OLs at different stages of differentiation  hasrevealed significant enrichment in genes coding for proteinsof the SWI/SNF remodeling complex during the transitionfrom OPCs to immature OLs . In particular,in response to differentiation signals, a significant increasein the RNAPII amount was registered on exons of the Brg1 gene (encoding the core ATPase of the SWI/SNF complex)but was not observed on the gene of its only homolog, Brm.During early embryonic development , Brg1 transcripts are virtually undetectable in proliferatingneuronal stem cells (NSCs) of the ventricular zone (VZ) inthe mouse forebrain, in contrast to the already differentiatedpostmitotic cells of the mantle zone .This pattern of Brg1 expression changes after E13, in such away that most VZ cells become Brg1-immunoreactive , in good agreement with the data on thebeginning of the first wave of OPC specification in mice onE12.5 during this period . A Cre-mediatedknockout involving a conditional deletion of Brg1 under thecontrol of nestin (an NSC marker) in mice leads to a decrease in the number of proliferatingNSCs capable of subsequently undergoing gliogenesis.It is assumed that this phenomenon can be mediated by stemcell differentiation into postmitotic cells (neurons) and/or byapoptosis. Those authors believe that Brg1 keeps NSCs in anundifferentiated state until they respond to some gliogenicsignals during development in mammals .An increase in the transcription of Brg1 has been notedexclusively during the transition from precursors to immatureOLs and is not observed during differentiation of othercell types, suggesting that this is a unique event initiatingoligodendrocytic differentiation. Western blotting and immunohistochemicalresults also indicate that Brg1 expressionis mainly limited to differentiating oligodendrocytic cells . By contrast, in another study, according to immunohistochemicalfindings, Brg1 expression was detectableat all stages of OL development, and there was no obviousdifference in staining intensity between OPCs and maturingOLs , a myelination-deficient phenotypemanifests itself, although the number of OPCs and their proliferationrate are comparable to those in control mice. It turnsout that these mice feature increased expression levels of differentiationinhibitors  anddownregulation of genes associated with both the synthesisof lipids and myelin sheath proteins and with differentiationregulation (Gm98/MRF and Sox10) . In theaforementioned work of M. Bischof and coworkers (2015), itwas also found that early deletion of Brg1 (with Cre under thecontrol of Brn4 expressed in NSCs) throughout the ventricularzone of the spinal cord also prevents Sox10 expression inOLPs until the end of embryogenesis.ChIP-seq with antibodies to Brg1 revealed an order ofmagnitude more peaks in immature OLs than in OPCs, whilealmost all the peaks in OPCs overlapped with the peaks ofimmature OLs but had significantly lower intensity. Geneanalysis showed that Brg1 target genes are mainly associatedwith myelination, oligodendrocytic differentiation, andcell cycle arrest . Thoseauthors hypothesized that Brg1 mainly targets intergenic enhancer regions because ~80 % of peaks of Brg1 binding inimmature OLs were located at a considerable distance froma transcription start site .Transcription factor Olig2 is thought to play an importantrole in the regulation of Brg1 functions in oligodendrogenesis.It is reported that Olig2 not only regulates Brg1 expressionbut also recruits the SWI/SNF complex with the Brg1 ATPaseto OL-specific enhancers during the critical transition fromOPCs to immature OLs; as a consequence, directed chromatinremodeling ensues, which is necessary for activation of theoligodendrocytic differentiation program .Moreover, it has been revealed that at early stages of development(E14.5), Brg1 within the SWI/SNF complex interactswith the proximal promoter of the Olig2 gene in corticalNSCs and suppresses its expression, whereas in cells of theventricular zone, where oligodendrocytic differentiation isseen first, no suppressive effect of Brg1 on Olig2 was found.Therefore, all these data indicate that Brg1, which is a partof the SWI/SNF complex, is required for both OPC specificationand oligodendrocytic differentiationSubfamily CHDATPases of this subfamily of remodelers are representedby nine proteins, CHD1–9, which differ in their domainorganization. The complexes formed by them can combine1 to 10 subunits. Some of them shift or push nucleosomes tofacilitate transcription, whereas others play a repressive part, and thus are important regulators ofcell differentiation . It has been demonstratedthat chromodomain ATPases Chd7 and Chd8 are importantfor the initiation of the processes of nerve-fiber myelinationas well as remyelination in the pathogenesis of some disorders.Chd7 expression is present in most of oligodendrocytic cellsin a number of structures within a developing brain  and in the spinal cord. A substantial proportionof these cells are differentiated OLs with Chd7 overexpression,whereas in OPCs, Chd7 expression is reported tobe lower . A conditional knockout of the Chd7gene using the Olig1–Cre construct reduces the number of OLsexpressing MBP both at embryonic and early postnatal stagesof development and decreases the expression of basic myelinproteins Mbp and Plp1 at the mRNA level. As a result, in themutant animals, there is a decrease of white-matter volumein the brain and impaired myelination of nerve fibers (a lowerg-ratio) in comparison with control animals (PND14). In thecerebral cortex, the Chd7 deletion also leads to a decreasein the number of mature OLs at the early postnatal stages ofdevelopment but does not have a significant impact on thenumber of OPCs and their proliferation. Nevertheless, withage, mutant mice showed a gradually rising number of matureOLs, and by PND60, the degree of myelination in the spinalcord approached normal. Accordingly, Chd7 is necessary forthe initiation of oligodendrocytic differentiation, and Chd7 losscauses a noticeable delay in the myelination of nerve fibers.A comparative analysis of gene expression profiles in the spinalcord between control mice and mice with the conditional Chd7 knockout (PND8) confirmed the importance of Chd7 forthe regulation of genes responsible for the differentiation intoOLs and for myelination; furthermore, in most cases (~84 %),it functions as a transcriptional activator .Normally, in adult mice, Chd7 expression in the whitematter of the spinal cord is practically undetectable; however,lysolecithin-induced demyelination causes local re-expressionof Chd7 against the background of myelin regeneration viaOPC recruitment. In the case of a Chd7 deletion in the affectedtissue area, there was a significant reduction not only in the OLnumber but also in the expression levels of Mbp and Plp1 ascompared to the control, and morphometric characteristics ofmyelinated fibers deteriorated. For these reasons, those authorsbelieve that Chd7 is crucial for remyelination in case of whitematterdamage . Chd7 has been reported tobe a key regulator of OPC activation and proliferation afterspinal cord injury .In the expression regulation of the Chd7 gene itself, an importantrole is played by the Brg1 remodeler, the conditionalknockout of which significantly suppresses Chd7 expressionin mutant mice. Furthermore, within the Chd7 gene, multiplesites of cooperative binding of factors Brg1 and Olig2 havebeen identified, and these sites are functionally significant atthe stage of OPCs and immature OLs A genome-wide search for Chd7-binding sites by ChIP-seqin differentiating OLs has shown that they are predominantlylocated in the region +5 kbp relative to a transcription startsite of target genes and also serve as binding sites for transcriptionfactor Olig2, which is known to regulate enhancersthat are functionally important for oligodendrogenesis, inparticular, by recruiting Brg1 to them .A comparative analysis of distributions of ChIP-seq peaksfor the remodelers Chd7 and Brg1 revealed that the peaksdo not overlap in ~76 % of cases, and therefore Chd7 hasunique molecular functions that control OL maturation .CHD7 mutations cause human CHARGE syndrome, whichis characterized by multiple pathologies including craniofacialanomalies, neurological dysfunction, and growth retardation.Most CHARGE patients show some degree of intellectualdisability, and many have structural aberrations of the corpuscallosum and cerebellar vermis .Subfamily INO80/SWRThe remodeling complexes belonging to this subfamily cancontain more than 10 subunits and perform a variety of functions,including facilitation of transcription activation andDNA repair . In one study , it was demonstrated that a member of this family,chromatin-remodeling complex TIP60/EP400, is an importantcomponent of the oligodendrocytic differentiation program.It turned out that a Cre-mediated knockout of Ep400 (coreATPase) at various oligodendrogenesis stages in transgenicmice does change the OPC number but is the reason for a sharpdrop in the number of OLs that started terminal differentiationand initiated myelin gene expression.Analysis of gene expression in the OLs from mice with theEp400 knockout confirmed downregulation of not only terminal differentiation and myelination genes, such as Plp1, Mbp,Mog, and Nfasc, but also key components of the transcriptionalnetwork, e.g., Sox10, Nkx2.2, Olig2, Olig1, Myrf, and Fyn, theproducts of which regulate the processes of oligodendrocyticdifferentiation and myelination. In particular, in immatureOLs, EP400 specifically binds to the promoter and enhancerECR9 in the first intron of the Myrf gene and i) catalyzes thereplacement of histone H2A by the specialized H2A.Z histonein many nucleosomes as well as ii) recruits the Sox10transcription factor, with which EP400 physically interacts toactivate Myrf expression during oligodendrocytic differentiation.After the differentiation, EP400 induces changes in thepattern of H2A.Z localization on the promoter.Additionally, in cultured primary OLs, it was found thatthe absence of EP400 impairs repair processes, as evidencedby an increase in the amount of histone γH2A.X, which is amarker of a double-stranded DNA break and emerges as aresult of phosphorylation of the specialized H2A.X histone.Because such breaks are a signal for apoptosis, it is possibleto define EP400 as a factor that promotes OL survival andprotects DNA from damage or helps with its repair . Given that upon completion of the differentiationinto OLs and at initial stages of myelination, there is anincrease in heterochromatinization and nuclear condensation, it can be theorized that such criticalchanges in the structure of chromatin make it especially vulnerableduring this period of oligodendrogenesis and requiremore attention from a “surveillance” system .Thus, EP400 is not required for OPC specification or forearly development of clones in embryogenesis but is necessaryduring terminal oligodendrocytic differentiation and theactive phase of myelination.Each stage of oligodendrogenesis is accompanied by a changein the expression of a large number of genes. The activationof some genes and the repression of others are implementedby precisely spatially and temporally coordinated interactionsof various transcription factors with the promoters and enhancersof these genes. Such fine regulation is possible due tothe coordinated fine-tuned work of transcription factors andATP-dependent chromatin-remodeling complexes, which determinethe regulatory landscape of chromatin and contributeto its epigenetic modifications . In additionto many common properties among all chromatin remodelers,they have distinct features that explain their functionalspecialization in the cell , in particular,at different stages of differentiation in oligodendrogenesis.It has been shown that OP specification requires SWI/SNFcomplexes, which keep NSCs in an undifferentiated state untilthey respond to certain gliogenic signals. Besides, membersof this subfamily are curators of transcriptional activity ofgenes at all stages of oligodendrocytic differentiation. By contrast,CHD7 is required for OPC proliferation, for the onsetof oligodendrocytic differentiation, and for the activation ofgenes responsible for myelination and remyelination, whereasEP400 is necessary only for terminal oligodendrocytic differentiationand the active phase of myelination .The roles of ISWI subfamily members in oligodendrogenesishave not yet been investigated; however, given theirfunctional feature – the assembly and positioning of nucleosomes – it ispossible that they are important for heterochromatinizationprocesses, which intensify with the gradual transition fromOPCs to mature myelinating OLs, and for nuclear condensation.The authors declare no conflict of interest.Bargaje R., Alam M.P., Patowary A., Sarkar M., Ali T., Gupta S.,Garg M., Singh M., Purkanti R., Scaria V., Sivasubbu S., BrahmachariV., Pillai B. Proximity of H2A.Z containing nucleosome to thetranscription start site influences gene expression levels in the mammalianliver and brain. 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