| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Genetics and Molecular Biology |
Department of Biochemistry, Microbiology and Immunology, University of Ottawa, 451 Smyth Road, Ottawa, ON, K1H 8M5, Canada1
Department of Microbiology, University of Guelph, Guelph, ON, N1G 2W1, Canada2
Author for correspondence: Jo-Anne R. Dillon. Tel: +1 613 562 5459. Fax: +1 613 562 5452. e-mail: jdillon{at}uottawa.ca
The minCDE genes involved in division site selection in Neisseria gonorrhoeae were identified using raw data from the N. gonorrhoeae genome project and are part of a cluster of 27 genes. When gonococcal min genes were heterologously expressed as a cluster in Escherichia coli, minicells and filaments were produced, indicating that gonococcal min genes disrupted cell division in other genera. The insertional inactivation of the minC gene of N. gonorrhoeae CH811 resulted in a strain (CSRC1) with decreased viability and grossly abnormal cell division as observed by phase-contrast and electron microscopy analysis. Western blot analysis of N. gonorrhoeae CSRC1 confirmed that MinCNg was not produced. Complementation of CSRC1 by integrating a minC–6xHis tag fusion at the proAB locus by homologous recombination restored viability and 1·9 times wild-type levels of MinCNg expression. This slight increase of expression caused a small percentage of the complemented cells to divide aberrantly. This suggested that the 6xHis tag has partially affected the stability of MinC, or that the chromosomal position of minC is critical to its regulation. Comparison of MinC proteins from different bacteria showed a homologous region corresponding to residues 135–230 with five conserved amino acids. Overexpression of MinCNg in wild-type E. coli cells induced filamentation and an E. coli minC mutant was successfully complemented with minCNg. Therefore, the evidence indicates that MinC from N. gonorrhoeae acts as a cell-division inhibitor and that its role is essential in maintaining proper division in cocci.
Keywords: Neisseria gonorrhoeae, minC, cell-division inhibitor, cell lysis, cocci
Abbreviations: Ap, ampicillin; Cm, chloramphenicol; GFP; green fluorescent protein; Kan, kanamycin; RT, reverse transcriptase; Str, streptomycin
This article has been cited by other articles:
|
|
 |
|
  J. Cheng, C. D. Sibley, R. Zaheer, and T. M. Finan A Sinorhizobium meliloti minE mutant has an altered morphology and exhibits defects in legume symbiosis Microbiology, February 1, 2007; 153(2): 375 - 387. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Ramirez-Arcos, M. Liao, S. Marthaler, M. Rigden, and J.-A. R. Dillon Enterococcus faecalis divIVA: an essential gene involved in cell division, cell growth and chromosome segregation Microbiology, May 1, 2005; 151(5): 1381 - 1393. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Ramirez-Arcos, V. Greco, H. Douglas, D. Tessier, D. Fan, J. Szeto, J. Wang, and J. R. Dillon Conserved Glycines in the C Terminus of MinC Proteins Are Implicated in Their Functionality as Cell Division Inhibitors J. Bacteriol., May 1, 2004; 186(9): 2841 - 2855. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Du and C. G. Arvidson Identification of ZipA, a Signal Recognition Particle-Dependent Protein from Neisseria gonorrhoeae J. Bacteriol., April 1, 2003; 185(7): 2122 - 2130. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. Kroos and J. R. Maddock Prokaryotic Development: Emerging Insights J. Bacteriol., February 15, 2003; 185(4): 1128 - 1146. [Full Text] [PDF]
|
|
|
|
|
|
J. Szeto, S. Ramirez-Arcos, C. Raymond, L. D. Hicks, C. M. Kay, and J.-A. R. Dillon Gonococcal MinD Affects Cell Division in Neisseria gonorrhoeae and Escherichia coli and Exhibits a Novel Self-Interaction J. Bacteriol., November 1, 2001; 183(21): 6253 - 6264. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| INT J SYST EVOL MICROBIOL | MICROBIOLOGY | J GEN VIROL |
| J MED MICROBIOL | ALL SGM JOURNALS | |
