1887

Abstract

The genes involved in division site selection in were identified using raw data from the genome project and are part of a cluster of 27 genes. When gonococcal genes were heterologously expressed as a cluster in , minicells and filaments were produced, indicating that gonococcal genes disrupted cell division in other genera. The insertional inactivation of the gene of 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 CSRC1 confirmed that MinC was not produced. Complementation of CSRC1 by integrating a –6×His tag fusion at the locus by homologous recombination restored viability and 19 times wild-type levels of MinC expression. This slight increase of expression caused a small percentage of the complemented cells to divide aberrantly. This suggested that the 6×His tag has partially affected the stability of MinC, or that the chromosomal position of 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 MinC in wild-type cells induced filamentation and an mutant was successfully complemented with . Therefore, the evidence indicates that MinC from acts as a cell-division inhibitor and that its role is essential in maintaining proper division in cocci.

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2001-01-01
2024-04-24
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