sfi-independent filamentation in Escherichia coli Is lexA dependent and requires DNA damage for induction

Hill, Thomas M.; Sharma, Bela; Valjavec-Gratian, Majda; Smith, Jim Q.

doi:10.1128/jb.179.6.1931-1939.1997

Cited by 69 publications

(66 citation statements)

References 45 publications

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“…As discussed above, SOS induction, as measured in luceriferase gene fusions (fold induction of SulA promoter 1.76 Ϯ 0.69), did not occur concomitant with ObgE depletion. Both SulA-dependent and SulA-independent filamentation have been observed to depend on RecA gene function (Hill et al, 1997). We found that cell filamentation in ObgE-depleted cells was not dependent on functional RecA.…”

Section: Inefficient Ftsz-ring Formation In Obge-depleted Cellssupporting

confidence: 50%

Chromosome segregation control by Escherichia coli ObgE GTPase

Foti

Persky²,

Ferullo

et al. 2007

Molecular Microbiology

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SummaryEscherichia coli cells depleted of the conserved GTPase, ObgE, show early chromosome-partitioning defects and accumulate replicated chromosomes in which the terminus regions are colocalized. Cells lacking ObgE continue to initiate replication, with a normal ratio of the origin to terminus. Localization of the SeqA DNA binding protein, normally seen as punctate foci, however, was disturbed. Depletion of ObgE also results in cell filamentation, with polyploid DNA content. Depletion of ObgE did not cause lethality, and cells recovered fully after expression of ObgE was restored. We propose a model in which ObgE is required to license chromosome segregation and subsequent cell cycle events.

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Section: Inefficient Ftsz-ring Formation In Obge-depleted Cellssupporting

confidence: 50%

Chromosome segregation control by Escherichia coli ObgE GTPase

Foti

Persky²,

Ferullo

et al. 2007

Molecular Microbiology

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“…This so-called sfi-independent pathway of cell filamentation is recA dependent (Burton and Holland, 1983;Hill et al, 1997). Since filamentation of the dnaAcos cells occurs independently of the functional recA gene, the CedA-linked pathway found in this work includes, at least, a novel step necessary for septum formation.…”

Section: Discussionmentioning

confidence: 68%

CedA is a novel Escherichia coli protein that activates the cell division inhibited by chromosomal DNA over‐replication

Katayama

Takata

Sekimizu

1997

Molecular Microbiology

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SummaryWe isolated and characterized a new gene related to the control of cell division regulation in Escherichia coli. At 30ЊC, the dnaAcos mutant causes over-replication of the chromosome, and colony formation is inhibited. We found that, at this temperature, the dnaAcos cells form filaments; therefore, septum formation is inhibited. This inhibition was independent of SfiA, an inhibitor of the septum-forming protein, FtsZ. To identify factors involved in this pathway of inhibition, we isolated seven multicopy suppressors for the cold-sensitive phenotype of the dnaAcos mutant. One of these proved to be a previously unknown gene, which we named cedA. This gene encoded a 12 kDa protein and resided at 38.9 min on the E. coli genome map. A multicopy supply of the cedA gene to the dnaAcos cells did not repress over-replication of the chromosome but did stimulate cell division of the host, the result being growth of cells with an abnormally elevated chromosomal copy number. Therefore, the expression level of the cedA gene seems to be important for inhibiting cell division of the dnaAcos mutant at 30ЊC. We propose that overreplication of the chromosome activates a pathway for inhibiting cell division and that the cedA gene modulates this division control. In the dnaA þ background, cedA also seems to affect cell division.

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“…Bacteria respond to stresses such as oxidative stress (8), nutrient stress (36), DNA damage (22), and some antibiotics (21,37) by arresting DNA replication and/or cell division. Filamentous uropathogenic Escherichia coli have been observed during infection of bladder epithelial cells (38).…”

Section: Discussionmentioning

confidence: 99%

“…Filamentous bacteria were observed using another Salmonella Typhimurium strain (14028s), indicating that filamentation is shared by more than one strain of Salmonella Typhimurium (data not shown). Filamentous bacteria had partial or absent septa, suggesting a defect in completion of cell division, an indicator of bacterial stress (21,22).…”

Section: Ifn-␥ Priming Of Raw 2647 Cells Restricts Salmonella Typhimmentioning

confidence: 99%

Macrophages Inhibit Salmonella Typhimurium Replication through MEK/ERK Kinase and Phagocyte NADPH Oxidase Activities

Rosenberger¹,

Finlay

2002

Journal of Biological Chemistry

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Host responses during the later stages of Salmonellamacrophage interactions are critical to controlling infection but have not been well characterized. After 24 h of infection, nearly half of interferon-␥-primed murine RAW 264.7 macrophage-like cells infected by Salmonella enterica serovar Typhimurium contained filamentous bacteria. Bacterial filamentation indicates a defect in completing replication and has been previously observed in bacteria responding to a variety of stresses. To understand whether macrophage gene expression was responsible for this effect on Salmonella Typhimurium replication, we used gene arrays to profile interferon-␥-primed RAW 264.7 cell gene expression following infection. We observed an increase in MEK1 kinase mRNA at 8 h, an increase in MEK protein at 24 h, and measured phosphorylation of MEK's downstream target kinase, ERK1/2, throughout the 24-h infection period. Treatment of cells with MEK kinase inhibitors significantly reduced numbers of filamentous bacteria observed within macrophages after 24 h and increased the number of intracellular colony-forming units. Phagocyte NADPH oxidase inhibitors and antioxidants also significantly reduced bacterial filamentation. Either MEK kinase or phagocyte oxidase inhibitors could be added 4 -8 h after infection and still significantly decrease bacterial filamentation. Oxidase activity appears to mediate bacterial filamentation in parallel to MEK kinase signaling, while inducible nitric-oxide synthase inhibitors had no significant effect on bacterial morphology. In summary, Salmonella Typhimurium infection of interferon-␥-primed macrophages triggers a MEK kinase cascade at later infection times, and both MEK kinase and phagocyte NADPH oxidase activity impair bacterial replication. These two signaling pathways mediate a host bacteriostatic pathway and may play an important role in innate host defense against intracellular pathogens.

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sfi-independent filamentation in Escherichia coli Is lexA dependent and requires DNA damage for induction

Cited by 69 publications

References 45 publications

Chromosome segregation control by Escherichia coli ObgE GTPase

Chromosome segregation control by Escherichia coli ObgE GTPase

CedA is a novel Escherichia coli protein that activates the cell division inhibited by chromosomal DNA over‐replication

Macrophages Inhibit Salmonella Typhimurium Replication through MEK/ERK Kinase and Phagocyte NADPH Oxidase Activities

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