Filamentation

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For other uses, see Filament (disambiguation).

A Bacillus cereus cell that has undergone filamentation following antibacterial treatment (upper
electron micrograph; top right) and regularly sized cells of untreated B. cereus (lower electron
micrograph)

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.[1] 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),[2] the increased cell length protecting bacteria
from protozoan predation and neutrophil phagocytosis by making ingestion of
the cells more difficult.[1][2][3][4] 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.[5][6] The number and length of
filaments within a bacterial population increases when the bacteria are treated
with various chemical and physical agents (eg. DNA synthesis-inhibiting
antibiotics, UV light).[2] Some of the key genes involved in filamentation in E.
coli include sulA and minCD.[7]

Contents

 1Filament formation
o 1.1Antibiotic-induced filamentation
o 1.2Ultraviolet light-induced filamentation
 o 1.3Nutrition-induced filamentation
 2See also
 3References

Filament formation[edit]
Antibiotic-induced filamentation[edit]
Some peptidoglycan synthesis inhibitors (eg. cefuroxime, ceftazidime) induce
filamentation by inhibiting the penicillin binding proteins (PBPs) responsible for
crosslinking peptidoglycan at the septal wall (eg. 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. [2][8]
DNA synthesis-inhibiting and DNA damaging antibiotics
(eg. 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.[2][9] If bacteria are deprived of the nucleobase thymine by
treatment with folic acid synthesis inhibitors (eg. trimethoprim), this also disrupts
DNA synthesis and induces SOS-mediated filamentation. Direct obstruction of
Z-ring formation by SulA and other FtsZ inhibitors (eg. berberine) induces
filamentation too.[2][10]
Some protein synthesis inhibitors (eg. kanamycin), RNA synthesis inhibitors
(eg. bicyclomycin) and membrane disruptors (eg. daptomycin, polymyxin B)
cause filamentation too, but these filaments are much shorter than the filaments
induced by the above antibiotics.[2]
Ultraviolet light-induced filamentation[edit]
UV light damages bacterial DNA and induces filamentation via the SOS
response.[2][11]
Nutrition-induced filamentation[edit]
Nutritional changes may also cause bacterial filamentation. [7] For example, if
bacteria are deprived of the nucleobase thymine by starvation, this disrupts
DNA synthesis and induces SOS-mediated filamentation. [2][12]

See also[edit]
 Bacterial morphological plasticity
 Segmented filamentous bacteria

References[edit]
1. ^ Jump up to:a b Jaimes-Lizcano YA, Hunn DD, Papadopoulos KD (April 2014).
"Filamentous Escherichia coli cells swimming in tapered microcapillaries". Research in
Microbiology.  165(3): 166–74. doi:10.1016/j.resmic.2014.01.007.  PMID  24566556.
2. ^ Jump up to:a b c d e f g h i Cushnie TP, O'Driscoll NH, Lamb AJ (December
2016).  "Morphological and ultrastructural changes in bacterial cells as an indicator of
antibacterial mechanism of action".  Cellular and Molecular Life Sciences. 73 (23): 4471–
4492. doi:10.1007/s00018-016-2302-2.  hdl:10059/2129. PMID 27392605.  S2CID 206582
1.
3. ^ Hahn MW, Höfle MG (May 1998). "Grazing Pressure by a Bacterivorous
Flagellate Reverses the Relative Abundance of Comamonas acidovorans PX54 and Vibrio
Strain CB5 in Chemostat Cocultures".  Applied and Environmental Microbiology.  64  (5):
1910–8.  doi:10.1128/AEM.64.5.1910-1918.1998.  PMC 106250. PMID 9572971.
4. ^ Hahn MW, Moore ER, Höfle MG (January 1999). "Bacterial filament formation, a
defense mechanism against flagellate grazing, is growth rate controlled in bacteria of
different phyla". Applied and Environmental Microbiology. 65 (1): 25–
35. doi:10.1128/AEM.65.1.25-35.1999.  PMC 90978. PMID 9872755.
5. ^ Justice SS, Hunstad DA, Cegelski L, Hultgren SJ (February 2008).
"Morphological plasticity as a bacterial survival strategy".  Nature Reviews.
Microbiology.  6 (2): 162–8. doi:10.1038/nrmicro1820.  PMID  18157153. S2CID  7247384.
6. ^ Fuchs BB, Eby J, Nobile CJ, El Khoury JB, Mitchell AP, Mylonakis E (June
2010).  "Role of filamentation in Galleria mellonella killing by Candida albicans". Microbes
and Infection.  12  (6): 488–
96. doi:10.1016/j.micinf.2010.03.001.  PMC 288367. PMID 20223293.
7. ^ Jump up to:a b Bi E, Lutkenhaus J (February 1993).  "Cell division inhibitors SulA and
MinCD prevent formation of the FtsZ ring".  Journal of Bacteriology. 175 (4): 1118–
25. doi:10.1128/jb.175.4.1118-1125.1993. PMC  193028.  PMID  8432706.
8. ^ Spratt BG (August 1975). "Distinct penicillin binding proteins involved in the
division, elongation, and shape of Escherichia coli K12".  Proceedings of the National
Academy of Sciences of the United States of America.  72  (8): 2999–
3003. doi:10.1073/pnas.72.8.2999.  PMC 432906. PMID 1103132.
9. ^ Cordell SC, Robinson EJ, Lowe J (June 2003).  "Crystal structure of the SOS cell
division inhibitor SulA and in complex with FtsZ". Proceedings of the National Academy of
Sciences of the United States of America.  100  (13): 7889–
94. doi:10.1073/pnas.1330742100. PMC  164683.  PMID  12808143.
10. ^ Ray S, Dhaked HP, Panda D (October 2014). "Antimicrobial peptide CRAMP (16-
33) stalls bacterial cytokinesis by inhibiting FtsZ assembly". Biochemistry.  53  (41): 6426–
9.  doi:10.1021/bi501115p.  PMID  25294259.
11. ^ Walker JR, Pardee AB (January 1968).  "Evidence for a relationship between
deoxyribonucleic acid metabolism and septum formation in Escherichia coli". Journal of
Bacteriology. 95 (1): 123–31. doi:10.1128/JB.95.1.123-
131.1968. PMC  251980.  PMID  4867214.
12. ^ Ohkawa T (December 1975). "Studies of intracellular thymidine nucleotides.
Thymineless death and the recovery after re-addition of thymine in Escherichia coli K
12". European Journal of Biochemistry. 60 (1): 57–66. doi:10.1111/j.1432-
1033.1975.tb20975.x.  PMID  1107038