Isolation and characterization of Tn917lac-generated competence mutants of Bacillus subtilis

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118

comK, which encodes the competence transcription factor, is itself transcriptionally activated at the transition from exponential growth to stationary phase in Bacillus subtilis. MecA, a negative regulator of competence, also inhibits comK transcription when overexpressed, and a mec4 null mutation results in comK overexpression. Although null mutations in mecA, as well as in another gene, mecB, are known to bypass the requirements for nearly all of the competence regulatory genes, the comK requirement is not suppressed by mecA inactivation. Various competence reulatory genes (comA srfA, degU, abrB, sin, and spoOA) are shown to be required for the expression of comK srfA transcription is shown to occur equally in cells destined for competence and those destined not to become competent. In contrast, comK transcription is restricted to the presumptive competent cells. These and other results are combined to describe a regulatory pathway for competence.

Section: Resultsmentioning

confidence: 99%

The regulation of competence transcription factor synthesis constitutes a critical control point in the regulation of competence in Bacillus subtilis

Hahn¹,

Kong²,

Dubnau³

1994

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118

“…comP is an essential competence gene that appears to encode the cognate sensor for comA (38), while degS (19,23) encodes a sensor that probably works together with the product of degU. Other regulatory genes that are required for the development of competence include spoOH (3,11), sin (12), and abrB (16,27). These specify known DNAbinding proteins and may be involved in the transcriptional control of competence.…”

mentioning

confidence: 99%

Growth medium-independent genetic competence mutants of Bacillus subtilis

Dubnau¹,

Roggiani²

1990

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The development of competence in Bacilus subtilis is normally dependent on the growth medium. Expression of late competence genes occurs in glucose-minimal salts-based media but not in complex media. Expression is also inhibited when glutamind is added to competence medium and when glycerol is substituted for glucose. Mutations have been identified in two regulatory loci, mecA and mecB, which render competence development independent of these variables. Although in mec mutants the expression of late competence genes, as weil as of competence itself, occurred in all media tested, this expression was still growth stage regulated. Thus at least some forms of medium-dependent and growth stage-specific regulation are genetically separable. One of the mecB mutations (mecB31) conferred oligosporogenicity. The mecB mutations were tightiy linked by transformation to rif, lpm, and std markers and were located between nif-2103 and cysA14. The mecA42 mutant was linked by transduction to argC4.

“…Mutations in kinA also cause a delay in sporulation and a decrease in the expression of several spoII genes (3,39). (20), genes controlled by eH (csh genes) (28), and genes controlled by &rB (csb genes) (6).…”

mentioning

confidence: 99%

Interactions among mutations that cause altered timing of gene expression during sporulation in Bacillus subtilis

Ireton

Grossman

1992

The ski4::Tn917lac insertion mutation in Bacillus subtilis was isolated in a screen for mutations that cause a defect in sporulation but that are suppressed by the presence or overexpression of the histidine protein kinase encoded by kinA (spoIIJ). ski4::Tn917lac caused a small defect in sporulation, but in combination with a null mutation in kinA, it caused a much more severe defect. The insertion mutation was in an 87-amino-acid open reading frame (orf87 bofA) that controls the activation of a sigma factor, sigma K, at intermediate times during sporulation. The ski4 mutation caused the premature expression of cotA, a gene controlled by sigma K. An independent mutation that causes the premature activation of sigma K also caused a synthetic (synergistic) sporulation phenotype in combination with a null mutation in kinA, indicating that the defect was due to altered timing of gene expression directed by sigma K. Expression of ski4 was shown to be controlled by the sporulation-specific sigma factor sigma E.