Central role for the Escherichia coli minC gene product in two different cell division-inhibition systems.

Boer, Piet A. J. de; Crossley, R.E.; Rothfield, Lawrence

doi:10.1073/pnas.87.3.1129

Cited by 151 publications

(144 citation statements)

References 17 publications

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“…The ssgA gene product, a small highly acidic protein localized in the cytoplasm, is not likely to be a component of the cell division machinery in the cell membrane and shows no sequence homology to FtsZ. It is possible that ssgA is functionally analogous to the minE gene of E. coli, which acts as a topological specificity factor in septum formation during cell division (de Boer et al, 1989(de Boer et al, , 1990, and that SsgA could interact with a division inhibitor present in Streptomyces ; thus overexpression would result in the observed fragmented growth. Further investigations into the functioning of the SsgA protein may provide important information on the mechanistic relationship between sporulation and cell division in Streptomyces, about which very little is currently known.…”

Section: Discussionmentioning

confidence: 99%

Expression analysis of the ssgA gene product, associated with sporulation and cell division in Streptomyces griseus

et al. 1997

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The ssgA gene of Streptomyces griseus B2682, when present in high copy number, results in both suppression of sporulation and fragmented growth of mycelia. Western analysis with polyclonal antibodies against the gene product (SsgA) revealed a close correlation between SsgA accumulation and the onset of sporulation in wild-type cells. The protein was only detected in the cytoplasm. Certain developmental mutants of S. griseus (afs, relC and brgA) which are defective in aerial mycelium formation in solid culture and submerged spore formation in liquid culture failed to accumulate SsgA. The SsgA protein appeared shortly (1 h) after nutritional shift-down of strain B2682 cells, afs mutant cells sporulated and expressed SsgA only when A-factor was present both before and after nutritional shift-down. Introduction of the ssgA gene in a low-copy-number vector into strain B2682 resulted in fivefold overexpression of SsgA, and was accompanied by fragmented growth of mycelia and suppression of submerged spore formation (in liquid culture) and aerial mycelium formation (in solid culture). Streptomycin production was not inhibited. In a control experiment, a nonfunctional ssgA gene possessing a frameshift mutation near its N-terminus had no effect on either growth or sporulation. It is proposed that the ssgA gene product plays a role in promoting the developmental process of S. griseus.

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Section: Discussionmentioning

confidence: 99%

Expression analysis of the ssgA gene product, associated with sporulation and cell division in Streptomyces griseus

et al. 1997

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“…MinC-DicB, like MinC-MinD, cause division inhibition in vivo, which has suggested a central role of MinC in the division inhibition process (5). However, in contrast to MinD inhibition, DicB-dependent inhibition is insensitive to MinE (5). A model for the interactions of min and dic gene products and their effect on division positioning is shown in Fig.…”

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New minC mutations suggest different interactions of the same region of division inhibitor MinC with proteins specific for minD and dicB coinhibition pathways

et al. 1992

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Proper positioning of division sites in Escherichia coli requires balanced expression of minC, minD, and minE gene products. Previous genetic analysis has shown that either MinD or an apparently unrelated protein, DicB, cooperates with MinC to inhibit division. We have isolated and sequenced minC mutations that suppress division inhibition caused by overproduction of either DicB or MinD proteins. Most missense mutations were located in the amino acid 160 to 200 region of MinC (231 amino acids). Some mutations exhibited preferential resistance to one or the other coinhibitor, suggesting that two distinct proteins, possibly MinD and DicB themselves, interact in slightly different manners with the same region of MinC to promote division inhibition.

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“…The target of the MinCD inhibitor appears to be FtsZ. Overproduction of FtsZ can induce minicell formation in wild-type cells (27) and suppress the inhibitory effect of excess MinCD (4,10). In addition, mutations in ftsZ, selected for resistance to sulA, confer resistance to MinCD, and one of these, which confers the greatest resistance to MinCD (ftsZ2 [Rsa]), leads to a minicell phenotype, even when it is not overexpressed (4,6).…”

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Cell division inhibitors SulA and MinCD prevent formation of the FtsZ ring

1993

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Immunoelectron microscopy was used to assess the effects of inhibitors of cell division on formation of the FtsZ ring in Eschlerichia coli. Induction of the cell division inhibitor SulA, a component of the SOS response, or the inhibitor MinCD, a component of the min system, blocked formation of the FtsZ ring and led to filamentation. Reversal of SulA inhibition by blocking protein synthesis in SulA-induced filaments led to a resumption of FtsZ ring formation and division. These results suggested that these inhibitors block cell division by preventing FtsZ localization into the ring structure. In addition, analysis of min mutants demonstrated that FtsZ ring formation was also associated with minicell formation, indicating that all septation events in E. coli involve the FtsZ ring.In Escherichia coli, cell division occurs near the midpoint of the long axis of the cell shortly after completion of chromosome replication (11). This temporal and spatial regulation of the cell division event is responsible for the narrow cell length distribution observed with exponentially growing cultures. In addition, the coordination of the cell division event with DNA segregation is responsible for the virtual absence of DNA-less cells in cultures. Under some conditions, however, this coordination between these two events is altered, leading to either inhibition of division or misplacement of the division event. Such disturbances of the coordination between the division event and DNA segregation lead to filamentation and/or production of anucleate cells, including minicells.Inhibition of cell division following interruption of DNA replication is due in part to the induction of sulA, a member of the SOS regulon (13, 14). SulA is thought to inhibit division by direct interaction with FtsZ, inhibiting its essential division activity (3,16,18). The inhibition is readily reversible, and division activity is restored as soon as SulA is removed, even without additional FtsZ synthesis (20).Proper placement of the division event is in part due to the min system, which is thought to prevent old sites (the cell poles) from being reused (25). In the absence of the min system, the poles become accessible to the division machinery, resulting in minicell production. The min system utilizes a bipartite division inhibitor, MinCD, and an additional gene product, MinE, that appears to confer topological specificity to the inhibitor (9). MATERIALS AND METHODS Bacterial strains, plasmids, and phage. The E. coli K-12 bacterial strains used in this study were derivatives of MC4100 (5) and BS100 (19). For examination of the effect of sulA, an MC4100 derivative containing plasmids pJF118EH (12) and pUGM470 (obtained from S. Gottesman) was used. The pJF118EH provides the lac repressor, and the pUGM470 has the sulA gene downstream of the lac promoter. BEF51 is an MC4100 derivative carrying a min deletion P1 transduced from PB114 (9). To examine the effects of minCD induction, BS100 containing XDB173, a transducing phage containing the minCD genes downstream ...

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Central role for the Escherichia coli minC gene product in two different cell division-inhibition systems.

Cited by 151 publications

References 17 publications

Expression analysis of the ssgA gene product, associated with sporulation and cell division in Streptomyces griseus

Expression analysis of the ssgA gene product, associated with sporulation and cell division in Streptomyces griseus

New minC mutations suggest different interactions of the same region of division inhibitor MinC with proteins specific for minD and dicB coinhibition pathways

Cell division inhibitors SulA and MinCD prevent formation of the FtsZ ring

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