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首页> 外文期刊>Journal of bacteriology >The Bacillus subtilis Extracytoplasmic Function σ Factor σV Is Induced by Lysozyme and Provides Resistance to Lysozyme
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The Bacillus subtilis Extracytoplasmic Function σ Factor σV Is Induced by Lysozyme and Provides Resistance to Lysozyme

机译：溶菌酶诱导枯草芽孢杆菌胞浆外功能σ因子σV并提供对溶菌酶的抗性

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Bacteria encounter numerous environmental stresses which can delay or inhibit their growth. Many bacteria utilize alternative σ factors to regulate subsets of genes required to overcome different extracellular assaults. The largest group of these alternative σ factors are the extracytoplasmic function (ECF) σ factors. In this paper, we demonstrate that the expression of the ECF σ factor σV in Bacillus subtilis is induced specifically by lysozyme but not other cell wall-damaging agents. A mutation in sigV results in increased sensitivity to lysozyme killing, suggesting that σV is required for lysozyme resistance. Using reverse transcription (RT)-PCR, we show that the previously uncharacterized gene yrhL (here referred to as oatA for O-acetyltransferase) is in a four-gene operon which includes sigV and rsiV. In quantitative RT-PCR experiments, the expression of oatA is induced by lysozyme stress. Lysozyme induction of oatA is dependent upon σV. Overexpression of oatA in a sigV mutant restores lysozyme resistance to wild-type levels. This suggests that OatA is required for σV-dependent resistance to lysozyme. We also tested the ability of lysozyme to induce the other ECF σ factors and found that only the expression of sigV is lysozyme inducible. However, we found that the other ECF σ factors contributed to lysozyme resistance. We found that sigX and sigM mutations alone had very little effect on lysozyme resistance but when combined with a sigV mutation resulted in significantly greater lysozyme sensitivity than the sigV mutation alone. This suggests that sigV, sigX, and sigM may act synergistically to control lysozyme resistance. In addition, we show that two ECF σ factor-regulated genes, dltA and pbpX, are required for lysozyme resistance. Thus, we have identified three independent mechanisms which B. subtilis utilizes to avoid killing by lysozyme.
机译：细菌遇到许多环境压力，这些环境压力可能会延迟或抑制其生长。许多细菌利用其他σ因子来调节克服不同细胞外攻击所需的基因子集。这些替代σ因子中最大的一组是胞外功能（ECF）σ因子。在本文中，我们证明了枯草芽孢杆菌中ECFσ因子σ V 的表达是由溶菌酶而不是其他破坏细胞壁的试剂特异性诱导的。 sigV 中的突变导致对溶菌酶杀伤的敏感性增加，这表明抗溶菌酶需要σ V 。使用逆转录（RT）-PCR，我们显示以前未鉴定的基因 yrhL （此处称为 O -乙酰基转移酶的 oatA ）是在包含 sigV 和 rsiV 的四基因操纵子中。在定量RT-PCR实验中，溶菌酶胁迫诱导 oatA 的表达。燕麦A 的溶菌酶诱导取决于σ V 。 sigV 突变体中过高的 oatA 表达可将溶菌酶抗性恢复至野生型水平。这表明OatA是依赖σ V 的溶菌酶抗性所必需的。我们还测试了溶菌酶诱导其他ECFσ因子的能力，发现只有 sigV 的表达是溶菌酶可诱导的。但是，我们发现其他ECFσ因子也导致了溶菌酶抗性。我们发现单独的 sigX 和 sigM 突变对溶菌酶抗性的影响很小，但与 sigV 突变结合使用时，溶菌酶的敏感性比 sigV 突变。这表明 sigV ， sigX 和 sigM 可能协同作用来控制溶菌酶抗性。此外，我们表明溶菌酶抗性需要两个ECFσ因子调节的基因 dltA 和 pbpX 。因此，我们确定了枯草芽孢杆菌用来避免溶菌酶杀死的三种独立机制。

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