Septation: Difference between revisions

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==Regulation {{HelpIcon|Help:Processes}}==
==Regulation {{HelpIcon|Help:Processes}}==
Z ring formation can be inhibited by sulA (recA- dependent SOS response) or by the action of the Min system<ref name='PMID:17085577'/>.   
Z ring formation can be inhibited by SulA (via recA-dependent SOS response) or by the action of the Min system<ref name='PMID:17085577'/><ref name='PMID: 8432706'/>.   
SOS gets triggered in response to DNA damage.  ''sulA'' is one of many genes whose expression gets upregulates upon LexA repressor cleavage<ref name='PMID:9068638'/>.  The SulA protein directly binds to monomeric FtsZ and inhibits its polymerization<ref name='PMID:12808143'/>.
SOS gets triggered in response to DNA damage.  ''sulA'' is one of many genes whose expression gets upregulates upon LexA repressor cleavage<ref name='PMID:9068638'/>.  The SulA protein directly binds to monomeric FtsZ and inhibits its polymerization<ref name='PMID:12808143'/>.


Revision as of 18:41, 4 June 2010

General Description

Invagination of the inner and outer membranes, as well as the cell wall that occurs to separate daughter cells. There are 4 main steps:

  • Selection of the division site
  • Recruitment of the septal proteins to the division site and formation of the ring
  • Constriction of the membrane and cell wall
    • Tetart et al. (1992) determined that cell division is not coupled to termination of replication, but to the segregation of the chromosomes[1].
    • GTP-dependent activation stage and hydrolysis stage[2][3]
  • Separation of the 2 daughter cells

Components

FtsZ(Z ring)[4], FtsA, FtsK, FtsN[5], FtsI, FtsE, FtsX, etc.


In order to ensure the chromosome doesn't get guillotined, TopoIV and the XerCD recombinase are also localized to the septa, via FtsK, but they are not involved directly in the membrane closure.

[6]

Some of the experiments that helped to order the components of this recruitment pathway can be found in Chen et al. (1999)[7], Weiss et al. (1999)[8], Ghigo et al. (1999)[9], and Mercer and Weiss (2002)[10].

Function

Regulation

Z ring formation can be inhibited by SulA (via recA-dependent SOS response) or by the action of the Min system[11][12]. SOS gets triggered in response to DNA damage. sulA is one of many genes whose expression gets upregulates upon LexA repressor cleavage[13]. The SulA protein directly binds to monomeric FtsZ and inhibits its polymerization[14].

Cell Biology

Experimental Resources

Comparison with other organisms

Notes

References

See Help:References for how to manage references in EcoliWiki.

  1. ↑ Pla, J et al. (1991) Preferential cytoplasmic location of FtsZ, a protein essential for Escherichia coli septation. Mol. Microbiol. 5 1681-6 PubMed
  2. ↑ de Boer, P et al. (1992) The essential bacterial cell-division protein FtsZ is a GTPase. Nature 359 254-6 PubMed
  3. ↑ RayChaudhuri, D & Park, JT (1992) Escherichia coli cell-division gene ftsZ encodes a novel GTP-binding protein. Nature 359 251-4 PubMed
  4. ↑ Dai, K & Lutkenhaus, J (1991) ftsZ is an essential cell division gene in Escherichia coli. J. Bacteriol. 173 3500-6 PubMed
  5. ↑ Addinall, SG et al. (1997) FtsN, a late recruit to the septum in Escherichia coli. Mol. Microbiol. 25 303-9 PubMed
  6. ↑ Geissler, B & Margolin, W (2005) Evidence for functional overlap among multiple bacterial cell division proteins: compensating for the loss of FtsK. Mol. Microbiol. 58 596-612 PubMed
  7. ↑ Chen, JC & Beckwith, J (2001) FtsQ, FtsL and FtsI require FtsK, but not FtsN, for co-localization with FtsZ during Escherichia coli cell division. Mol. Microbiol. 42 395-413 PubMed
  8. ↑ Weiss, DS et al. (1999) Localization of FtsI (PBP3) to the septal ring requires its membrane anchor, the Z ring, FtsA, FtsQ, and FtsL. J. Bacteriol. 181 508-20 PubMed
  9. ↑ Ghigo, JM et al. (1999) Localization of FtsL to the Escherichia coli septal ring. Mol. Microbiol. 31 725-37 PubMed
  10. ↑ Mercer, KL & Weiss, DS (2002) The Escherichia coli cell division protein FtsW is required to recruit its cognate transpeptidase, FtsI (PBP3), to the division site. J. Bacteriol. 184 904-12 PubMed
  11. ↑ Shiomi, D & Margolin, W (2007) The C-terminal domain of MinC inhibits assembly of the Z ring in Escherichia coli. J. Bacteriol. 189 236-43 PubMed
  12. ↑ Bi, E & Lutkenhaus, J (1993) Cell division inhibitors SulA and MinCD prevent formation of the FtsZ ring. J. Bacteriol. 175 1118-25 PubMed
  13. ↑ Hill, TM et al. (1997) sfi-independent filamentation in Escherichia coli Is lexA dependent and requires DNA damage for induction. J. Bacteriol. 179 1931-9 PubMed
  14. ↑ Cordell, SC et al. (2003) Crystal structure of the SOS cell division inhibitor SulA and in complex with FtsZ. Proc. Natl. Acad. Sci. U.S.A. 100 7889-94 PubMed
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