首页> 外文期刊>The Journal of toxicological sciences >Requirement of peroxiredoxin on the stationary phase of yeast cell growth
【24h】

Requirement of peroxiredoxin on the stationary phase of yeast cell growth

机译:过氧化物酶对酵母细胞生长稳定期的要求

获取原文
获取原文并翻译 | 示例
           

摘要

Toxic chemicals often induce reactive oxygen species (ROS). Although one of the most abundant ROS-sensitive proteins is in the peroxiredoxin (Prx) family, the function of Prx proteins is poorly understood because they are inactivated under high concentrations of hydrogen peroxide. Like mammalian cells, the model eukaryote Saccharomyces cerevisiae possesses multiple Prx proteins. Among the five Prx family proteins, Tsa1 and Ahp1 have the highest and second-highest expression levels, respectively. Here, we focused on a previously uncharacterized phenotype resulting from Tsa1 loss: impaired growth during the late exponential phase. We overexpressed catalase (CTT1) and Ahp1 in cells with disruptions in TSA1 and its homologue, TSA2 (tsa1/2Δ cells), and we found that neither Ctt1 nor Ahp1 overexpression suppressed the impaired cell growth at the stationary phase, although the ROS levels were successfully suppressed. Furthermore, the cell cycle profile was not altered by Tsa1/2 loss, at least in the late exponential phase; however, the glucose consumption rate slowed in the late exponential phase. Our results suggest that ROS levels are not responsible for the growth phenotype. Tsa1 might have a specific function that could not be replaced by Ahp1.
机译:有毒化学物质通常会诱发活性氧(ROS)。尽管最丰富的ROS敏感蛋白之一是过氧化物酶(Prx)家族,但对于Prx蛋白的功能却知之甚少,因为它们在高浓度的过氧化氢中会失活。像哺乳动物细胞一样,真核生物酿酒酵母模型具有多种Prx蛋白。在这五个Prx家族蛋白中,Tsa1和Ahp1分别具有最高和第二高的表达水平。在这里,我们集中于由Tsa1丢失导致的先前未表征的表型:指数后期的生长受损。我们在含有TSA1及其同系物TSA2(tsa1 /2Δ细胞)破坏的细胞中过表达过氧化氢酶(CTT1)和Ahp1,我们发现Ctt1和Ahp1均未抑制固定相细胞的生长受损,尽管ROS水平为成功地被压制。此外,至少在指数后期,Tsa1 / 2丢失不会改变细胞周期。但是,在指数后期,葡萄糖消耗速率减慢了。我们的结果表明,ROS水平与生长表型无关。 Tsa1可能具有无法被Ahp1取代的特定功能。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号