Staphylococcus aureus competence genes: mapping of the SigH, ComK1 and ComK2 regulons by transcriptome sequencing
Staphylococcus aureus competence genes: mapping of the SigH, ComK1 and ComK2 regulons by transcriptome sequencing
复制标题
DOI：
10.1111/mmi.12767
复制
发表时间：
2014-11-01
影响因子：
3.6
通讯作者：
Havarstein, Leiv Sigve
中科院分区：
文献类型：
--
作者：
Fagerlund, Annette;Granum, Per Einar;Havarstein, Leiv Sigve
金黄色葡萄球菌是一种主要的人类病原体。由甲氧西林耐药菌株（MRSA）引起的医院感染尤其令人关注，MRSA通过水平基因转移（HGT）获得了对广谱抗生素的耐药性。在金黄色葡萄球菌中，毒力和抗生素抗性基因通常编码在由HGT传播的移动的遗传元件上。结合和噬菌体转导早已被认为介导了该物种的HGT，但目前还不清楚天然遗传转化是否对该过程有显着贡献。最近，据报道，表达的替代西格玛因子SigH诱导的主管状态在金黄色葡萄球菌。然而，所获得的转化效率极低，这表明尚未发现感受态发育的最佳条件，因此我们使用转录组测序来确定已知在其他自然可转化细菌中感受态所需的全套基因是否是SigH调节子的一部分。我们的研究结果表明，一些必需的感受态基因不受SigH控制。这大概解释了先前报道的低转化效率，并表明必须涉及额外的调节机制。我们发现其中一种机制涉及ComK1，这是一种与SigH协同作用的转录激活因子。
Staphylococcus aureus is a major human pathogen. Hospital infections caused by methicillin-resistant strains (MRSA), which have acquired resistance to a broad spectrum of antibiotics through horizontal gene transfer (HGT), are of particular concern. In S.aureus, virulence and antibiotic resistance genes are often encoded on mobile genetic elements that are disseminated by HGT. Conjugation and phage transduction have long been known to mediate HGT in this species, but it is unclear whether natural genetic transformation contributes significantly to the process. Recently, it was reported that expression of the alternative sigma factor SigH induces the competent state in S.aureus. The transformation efficiency obtained, however, was extremely low, indicating that the optimal conditions for competence development had not been found. We therefore used transcriptome sequencing to determine whether the full set of genes known to be required for competence in other naturally transformable bacteria is part of the SigH regulon. Our results show that several essential competence genes are not controlled by SigH. This presumably explains the low transformation efficiency previously reported, and demonstrates that additional regulating mechanisms must be involved. We found that one such mechanism involves ComK1, a transcriptional activator that acts synergistically with SigH.