Chan P F, Foster S J
Department of Molecular Biology and Biotechnology, University of Sheffield, Sheffield S10 2TN, United Kingdom.
J Bacteriol. 1998 Dec;180(23):6232-41. doi: 10.1128/JB.180.23.6232-6241.1998.
The staphylococcal accessory regulator (encoded by sarA) is an important global regulator of virulence factor biosynthesis in Staphylococcus aureus. To further characterize its role in virulence determinant production, an sarA knockout mutant was created by insertion of a kanamycin antibiotic resistance cassette into the sarA gene. N-terminal sequencing of exoproteins down-regulated by sarA identified several putative proteases, including a V8 serine protease and a novel metalloprotease, as the major extracellular proteins repressed by sarA. In kinetic studies, the sarA mutation delays the onset of alpha-hemolysin (encoded by hla) expression and reduces levels of hla to approximately 40% of the parent strain level. Furthermore, SarA plays a role in signal transduction in response to microaerobic growth since levels of hla were much lower in a microaerobic environment than after aerobic growth in the sarA mutant. An exoprotein exhibiting hemolysin activity on sheep blood, and up-regulated by sarA independently of the accessory gene regulator (encoded by agr), was specifically induced microaerobically. Transcriptional gene fusion and Western analysis revealed that sarA up-regulates both toxic shock syndrome toxin 1 gene (tst) expression and staphylococcal enterotoxin B production, respectively. This study demonstrates the role of sarA as a signal transduction regulatory component in response to aeration stimuli and suggests that sarA functions as a major repressor of protease activity. The possible role of proteases as regulators of virulence determinant stability is discussed.
葡萄球菌辅助调节因子(由sarA编码)是金黄色葡萄球菌毒力因子生物合成的重要全局调节因子。为了进一步表征其在毒力决定因素产生中的作用,通过将卡那霉素抗生素抗性盒插入sarA基因,构建了一个sarA基因敲除突变体。对受sarA下调的外蛋白进行N端测序,鉴定出几种假定的蛋白酶,包括一种V8丝氨酸蛋白酶和一种新型金属蛋白酶,它们是受sarA抑制的主要细胞外蛋白。在动力学研究中,sarA突变延迟了α-溶血素(由hla编码)表达的起始,并将hla水平降低至亲本菌株水平的约40%。此外,SarA在响应微需氧生长的信号转导中起作用,因为在微需氧环境中hla的水平比sarA突变体在需氧生长后的水平低得多。一种对绵羊血表现出溶血素活性且受sarA独立于辅助基因调节因子(由agr编码)上调的外蛋白,在微需氧条件下被特异性诱导。转录基因融合和Western分析表明,sarA分别上调了毒性休克综合征毒素1基因(tst)的表达和葡萄球菌肠毒素B的产生。本研究证明了sarA作为响应通气刺激的信号转导调节成分的作用,并表明sarA作为蛋白酶活性的主要抑制因子发挥作用。还讨论了蛋白酶作为毒力决定因素稳定性调节因子的可能作用。