Fzf1p regulates an inducible response to nitrosative stress in Saccharomyces cerevisiae

被引:55
|
作者
Sarver, A
DeRisi, J [1 ]
机构
[1] Univ Calif San Francisco, Dept Biochem & Biophys, San Francisco, CA 94143 USA
[2] Univ Calif San Francisco, Chem & Chem Biol Grad Program, San Francisco, CA 94143 USA
关键词
D O I
10.1091/mbc.E05-05-0436
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The mechanisms by which microorganisms sense and detoxify nitric oxide ((NO)-N-center dot) are of particular interest due to the central role this molecule plays in innate immunity. We investigated the genetic basis of inducible nitric oxide ((NO)-N-center dot) detoxification in Saccharomyces cerevisiae by characterizing the genome-wide transcriptional response to exogenously supplied (NO)-N-center dot. Exposure to the (NO)-N-center dot-generating compound dipropylenetriamine NONOate resulted in both a general stress response as well as a specific response characterized by the induction of a small set of genes, including the yeast flavohemoglobin YHB1, SSU1, and three additional uncharacterized open reading frames. Transcriptional induction of SSU1, which encodes a putative sulfite transporter, has previously been shown to require the zinc finger transcription factor Fzf1p. Deletion of Fzf1p eliminated the nitrosative stress-specific transcriptional response, whereas overexpression of Fzf1p recapitulated this response in the absence of exogenously supplied (NO)-N-center dot. A cis-acting sequence unique to the promoter regions of Fzf1p-dependent genes was found to be sufficient to activate reporter gene activity in an (NO)-N-center dot- and Fzf1p-dependent manner. Our results suggest that the presence of (NO)-N-center dot or (NO)-N-center dot derivatives activates Fzf1p leading to transcriptional induction of a discrete set of target genes that function to protect the cell from (NO)-N-center dot-mediated stress.
引用
收藏
页码:4781 / 4791
页数:11
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