Saccharomyces cerevisiae Genes Involved in Survival of Heat Shock

被引:57
|
作者
Jarolim, Stefanie [1 ]
Ayer, Anita [2 ]
Pillay, Bethany [2 ]
Gee, Allison C. [3 ]
Phrakaysone, Alex [3 ]
Perrone, Gabriel G. [3 ]
Breitenbach, Michael [1 ]
Dawes, Ian W. [2 ]
机构
[1] Salzburg Univ, Div Genet, Dept Cell Biol, A-5020 Salzburg, Austria
[2] Univ New S Wales, Sch Biotechnol & Biomol Sci, Sydney, NSW 2052, Australia
[3] Univ Western Sydney, Sch Sci & Hlth, Penrith, NSW 1797, Australia
来源
G3-GENES GENOMES GENETICS | 2013年 / 3卷 / 12期
基金
奥地利科学基金会; 澳大利亚研究理事会;
关键词
heat shock; genome-wide screen; Saccharomyces cerevisiae; tryptophan metabolism; DNA repair; REPLICATIVE LIFE-SPAN; PROTEIN-SYNTHESIS; OXIDATIVE-STRESS; ENVIRONMENTAL-CHANGES; TRANSCRIPTION FACTOR; CCR4-NOT COMPLEX; CELL-DEATH; YEAST; EXPRESSION; GENOME;
D O I
10.1534/g3.113.007971
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
The heat-shock response in cells, involving increased transcription of a specific set of genes in response to a sudden increase in temperature, is a highly conserved biological response occurring in all organisms. Despite considerable attention to the processes activated during heat shock, less is known about the role of genes in survival of a sudden temperature increase. Saccharomyces cerevisiae genes involved in the maintenance of heat-shock resistance in exponential and stationary phase were identified by screening the homozygous diploid deletants in nonessential genes and the heterozygous diploid mutants in essential genes for survival after a sudden shift in temperature from 30 to 50 degrees. More than a thousand genes were identified that led to altered sensitivity to heat shock, with little overlap between them and those previously identified to affect thermotolerance. There was also little overlap with genes that are activated or repressed during heat-shock, with only 5% of them regulated by the heat-shock transcription factor. The target of rapamycin and protein kinase A pathways, lipid metabolism, vacuolar H+-ATPase, vacuolar protein sorting, and mitochondrial genome maintenance/translation were critical to maintenance of resistance. Mutants affected in l-tryptophan metabolism were heat-shock resistant in both growth phases; those affected in cytoplasmic ribosome biogenesis and DNA double-strand break repair were resistant in stationary phase, and in mRNA catabolic processes in exponential phase. Mutations affecting mitochondrial genome maintenance were highly represented in sensitive mutants. The cell division transcription factor Swi6p and Hac1p involved in the unfolded protein response also play roles in maintenance of heat-shock resistance.
引用
收藏
页码:2321 / 2333
页数:13
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