Filamentation
Filamentation, also termed conditional 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 can protecting bacteria from protozoan predation and neutrophil phagocytosis by making ingestion of cells more difficult. Filamentation is also 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. Direct, extrinsic causes of filamentation. Filamentation can be induced by the inhibition of cell division via exposure to antibiotics that inhibit divisome assembly or septal peptidoglycan synthesis. 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. Bacteriophage infection can also result in filamentation via the expression of proteins that inhibit divisome assembly. 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. Stress-induced filamentation. Filamentation is often a consequence of environmental stress, or starvation, and has been observed in response to temperature shocks, low water availability, high osmolarity, extreme pH, and UV exposure. UV light damages bacterial DNA and induces filamentation via the SOS response. Starvation-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. Nutrient excess and filamentation. Several macronutrients and biomolecules can cause bacterial cells to filament, including several amino acids: glutamine , proline and arginine and branched-chain amino acids. Certain bacterial species will also filament as a result of a tendency to accumulate phosphate in the form of polyphosphate, which can chelate metal cofactors needed by division proteins. Intrinsic dysbiosis-induced filamentation. Filamentation can also be induced by other pathways affecting thymidylate synthesis. For instance, partial loss of dihydrofolate reductase (DHFR) activity causes reversible filamentation. DHFR has a critical role in regulating the amount of tetrahydrofolate which is essential for purine and thymidylate synthesis. DHFR activity can be inhibited by mutations or by high concentrations of the antibiotic trimethoprim (see antibiotic -induced filamentation above). Other The overcrowding of the periplasm or envelope can also which can prevent normal divisome function, resulting in filamentation. Filamentation and biotic interactions. Several examples of filamentation that results from biotic interactions between organisms have been reported. Filamentous cells are resistant to ingestion by bacterivores and environmental conditions generated during predation can trigger filamentation. Filamentation can also be induced by signalling factors produced by other bacteria. Agrobacterium spp. filaments in proximity to plant roots (Finer et al., 2001) while E. coli filaments when exposed to plant extracts.