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Involvement of Clostridium botulinum ATCC 3502 Sigma Factor K in Early-Stage Sporulation

机译：肉毒梭菌ATCC 3502 Sigma K因子参与早期孢子形成

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A key survival mechanism of Clostridium botulinum , the notorious neurotoxic food pathogen, is the ability to form heat-resistant spores. While the genetic mechanisms of sporulation are well understood in the model organism Bacillus subtilis , nothing is known about these mechanisms in C. botulinum. Using the ClosTron gene-knockout tool, sigK , encoding late-stage (stage IV) sporulation sigma factor K in B. subtilis , was disrupted in C. botulinum ATCC 3502 to produce two different mutants with distinct insertion sites and orientations. Both mutants were unable to form spores, and their elongated cell morphology suggested that the sporulation pathway was blocked at an early stage. In contrast, sigK -complemented mutants sporulated successfully. Quantitative real-time PCR analysis of sigK in the parent strain revealed expression at the late log growth phase in the parent strain. Analysis of spo0A , encoding the sporulation master switch, in the sigK mutant and the parent showed significantly reduced relative levels of spo0A expression in the sigK mutant compared to the parent strain. Similarly, sigF showed significantly lower relative transcription levels in the sigK mutant than the parent strain, suggesting that the sporulation pathway was blocked in the sigK mutant at an early stage. We conclude that σ~(K) is essential for early-stage sporulation in C. botulinum ATCC 3502, rather than being involved in late-stage sporulation, as reported for the sporulation model organism B. subtilis . Understanding the sporulation mechanism of C. botulinum provides keys to control the public health risks that the spores of this dangerous pathogen cause through foods.
机译：肉毒梭菌（一种臭名昭著的神经毒性食物病原体）的关键生存机制是形成耐热孢子的能力。虽然在模型生物枯草芽孢杆菌中已很好地了解了孢子形成的遗传机制，但对于肉毒梭菌中的这些机制一无所知。使用ClosTron基因敲除工具，在枯草芽孢杆菌ATCC 3502中破坏了编码枯草芽孢杆菌后期（IV期）孢子形成因子K的sigK，产生了两个具有不同插入位点和方向的突变体。两种突变体均不能形成孢子，且其细长的细胞形态表明孢子形成途径在早期被阻断。相反，sigK互补的突变体成功形成孢子。亲本菌株中sigK的实时定量PCR分析揭示了亲本菌株中log生长后期的表达。 sigK突变体和亲本中编码孢子形成主开关的spo0A的分析显示，与亲本菌株相比，sigK突变体中spo0A表达的相对水平显着降低。同样，sigF的sigK突变体中的相对转录水平明显低于亲本菌株，这表明sigK突变体中的孢子形成途径在早期被阻断。我们得出结论，σ（K）对于肉毒梭菌ATCC 3502中的早期孢子形成是必不可少的，而不是如孢子形成模型生物枯草芽孢杆菌所报道的那样，参与后期孢子形成。了解肉毒梭菌的孢子形成机制提供了控制这种危险病原体的孢子通过食物引起的公共健康风险的关键。

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