Analysis of Saccharomyces cerevisiae null allele strains identifies a larger role for DNA damage versus oxidative stress pathways in growth inhibition by selenium.
Analysis of Saccharomyces cerevisiae null allele strains identifies a larger role for DNA damage versus oxidative stress pathways in growth inhibition by selenium.
复制标题
对酿酒酵母无效等位基因菌株的分析发现，DNA 损伤相对于氧化应激途径在硒抑制生长中发挥更大的作用。
DOI：
10.1002/mnfr.200700347
复制
发表时间：
2008
影响因子：
5.2
通讯作者：
Kinzy,TerriGoss
中科院分区：
文献类型：
--
作者：
Seitomer,Eden;Balar,Bharvi;He,Dongming;Copeland,PaulR;Kinzy,TerriGoss
Selenium toxicity is a growing environmental concern due to widespread availability of high‐dose selenium supplements and the development of high‐selenium agricultural drainage basins. To begin to analyze the effects of selenium toxicity at the genetic level, we have systematically determined which genes are involved in responding to high environmental selenium using a collection of viable haploid null allele strains ofSaccharomyces cerevisiaerepresenting three major stress pathways: theRAD9‐dependent DNA repair pathway, theRAD6/RAD18DNA damage tolerance pathway, and the oxidative stress pathway. A total of 53 null allele strains were tested for growth defects in the presence of a range of sodium selenite and selenomethionine (SeMet) concentrations. Our results show that ∼︁64–72% of the strains lackingRAD9‐dependent DNA repair orRAD6/RAD18DNA damage tolerance pathway genes show reduced growth in sodium seleniteversus∼︁28–36% in SeMet. Interestingly both compounds reduced growth in ∼︁21–25% of the strains lacking oxidative stress genes. These data suggest that both selenite and SeMet are likely inducing DNA damage by generating reactive species. The anticipated effects of loss of components of the oxidative stress pathway were not observed, likely due to apparent redundancies in these gene products that may keep the damaging effects in check.
