Filamentation

Filamentation is the anomalous growth of certain bacteria, such as "Escherichia coli", in which cells continue to elongate but do not divide (no septa formation). The cells that result from elongation without division have multiple chromosomal copies. In the absence of antibiotics or other stressors, filamentation occurs at a low frequency in bacterial populations (4-8% short filaments and 0-5% long filaments in 1- to 8-hour cultures), the increased cell length protecting bacteria from protozoan predation and neutrophil phagocytosis by making ingestion of the cells more difficult. Filamentation is also a virulence factor thought to protect bacteria from antibiotics, and is associated with other aspects of bacterial virulence such as biofilm formation. The number and length of filaments within a bacterial population increases when the bacteria are treated with various chemical and physical agents (e.g. DNA synthesis-inhibiting antibiotics, UV light). Some of the key genes involved in filamentation in "E. coli" include "sulA" and "minCD".
Filament formation.
Antibiotic-induced filamentation.
Some peptidoglycan synthesis inhibitors (e.g. cefuroxime, ceftazidime) induce filamentation by inhibiting the penicillin binding proteins (PBPs) responsible for crosslinking peptidoglycan at the septal wall (e.g. PBP3 in "E. coli" and "P. aeruginosa"). Because the PBPs responsible for lateral wall synthesis are relatively unaffected by cefuroxime and ceftazidime, cell elongation proceeds without any cell division and filamentation is observed.
DNA synthesis-inhibiting and DNA damaging antibiotics (e.g. metronidazole, mitomycin C, the fluoroquinolones, novobiocin) induce filamentation via the SOS response. The SOS response inhibits septum formation until the DNA can be repaired, this delay stopping the transmission of damaged DNA to progeny. Bacteria inhibit septation by synthesizing protein SulA, an FtsZ inhibitor that halts Z-ring formation, thereby stopping recruitment and activation of PBP3. If bacteria are deprived of the nucleobase thymine by treatment with folic acid synthesis inhibitors (e.g. trimethoprim), this also disrupts DNA synthesis and induces SOS-mediated filamentation. Direct obstruction of Z-ring formation by SulA and other FtsZ inhibitors (e.g. berberine) induces filamentation too.
Some protein synthesis inhibitors (e.g. kanamycin), RNA synthesis inhibitors (e.g. bicyclomycin) and membrane disruptors (e.g. daptomycin, polymyxin B) cause filamentation too, but these filaments are much shorter than the filaments induced by the above antibiotics.
Ultraviolet light-induced filamentation.
UV light damages bacterial DNA and induces filamentation via the SOS response.
Nutrition-induced filamentation.
Nutritional changes may also cause bacterial filamentation. For example, if bacteria are deprived of the nucleobase thymine by starvation, this disrupts DNA synthesis and induces SOS-mediated filamentation.