The whcA gene plays a negative role in oxidative stress response of Corynebacterium glutamicum
The whcA gene plays a negative role in oxidative stress response of Corynebacterium glutamicum
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DOI：
10.1111/j.1574-6968.2008.01398.x
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发表时间：
2009-01-01
影响因子：
2.1
通讯作者：
Lee, Heung-Shick
中科院分区：
文献类型：
--
作者：
Choi, Woon-Woo;Park, Soo-Dong;Lee, Heung-Shick
在这项研究中，我们分析了谷氨酸棒杆菌的WHCA基因，它编码WhiB家族蛋白的同源物。该基因的缺失不影响突变细胞的生长，说明WHCA基因在正常生长条件下不是必需的。然而，与野生型或Delta WHCA突变细胞相比，过表达该蛋白的细胞不仅显示出生长迟缓，而且对多种氧化剂，如联胺、甲萘二酮和过氧化氢的敏感性也有所增加。在WHCA过表达的细胞中，硫氧还蛋白还原酶的活性受到抑制，而在Delta WHCA突变株中，无论是否存在氧化应激，硫氧还蛋白还原酶的活性都受到抑制。WHCA基因在整个生长阶段都有结构性表达，其表达水平不受氧化胁迫的影响。用双向凝胶电泳法鉴定了一组受WHCA控制的蛋白质，分别命名为NADH氧化酶、乙醇脱氢酶、苯醌还原酶和半胱氨酸脱硫酶。相应的编码已鉴定蛋白的基因在Delta sigh突变细胞中没有转录。综上所述，这些数据表明，谷氨酸杆菌的WHCA基因在SIGH介导的应激反应途径中起着负面作用。
In this study, we analyzed the whcA gene from Corynebacterium glutamicum, which codes for a homologue of the WhiB-family of proteins. Deletion of the gene did not affect the growth of the mutant cells, indicating that the whcA gene was not essential under ordinary growth conditions. However, cells overexpressing the protein not only showed retarded growth as compared with the wild-type or the Delta whcA mutant cells but also showed increased sensitivity to a variety of oxidants, such as diamide, menadione, and hydrogen peroxide. Thioredoxin reductase activity was repressed in the whcA-overexpressing cells, whereas its activity in the Delta whcA mutant strain was derepressed regardless of the presence of oxidative stress. The whcA gene was constitutively expressed throughout the growth phase and its expression level was not affected by oxidative stress. A set of proteins under the control of whcA were identified by two-dimensional polyacrylamide gel electrophoresis and they were annotated as NADH oxidase, alcohol dehydrogenase, quinone reductase, and cysteine desulfurase. The corresponding genes encoding the identified proteins were not transcribed in Delta sigH mutant cells. Collectively, these data suggest that the whcA gene of C. glutamicum plays a negative role in the sigH-mediated stress response pathway.