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.
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Univ Calif Los Angeles, Ctr Hlth Sci, Sch Med, Dept Biol Chem, Los Angeles, CA 90095 USAUniv Calif Los Angeles, Ctr Hlth Sci, Sch Med, Dept Biol Chem, Los Angeles, CA 90095 USA
Treger, JM
Schmitt, AP
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Univ Calif Los Angeles, Ctr Hlth Sci, Sch Med, Dept Biol Chem, Los Angeles, CA 90095 USAUniv Calif Los Angeles, Ctr Hlth Sci, Sch Med, Dept Biol Chem, Los Angeles, CA 90095 USA
Schmitt, AP
Simon, JR
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Univ Calif Los Angeles, Ctr Hlth Sci, Sch Med, Dept Biol Chem, Los Angeles, CA 90095 USAUniv Calif Los Angeles, Ctr Hlth Sci, Sch Med, Dept Biol Chem, Los Angeles, CA 90095 USA
Simon, JR
McEntee, K
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Univ Calif Los Angeles, Ctr Hlth Sci, Sch Med, Dept Biol Chem, Los Angeles, CA 90095 USAUniv Calif Los Angeles, Ctr Hlth Sci, Sch Med, Dept Biol Chem, Los Angeles, CA 90095 USA
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Univ Manchester, Sch Biol Sci, Fac Biol Med & Hlth, Manchester Acad Hlth Sci Ctr, Oxford Rd, Manchester M13 9PT, Lancs, England
EBI, EMBL, Wellcome Trust Genome Campus, Cambridge CB10 1SD, EnglandUniv Manchester, Sch Biol Sci, Fac Biol Med & Hlth, Manchester Acad Hlth Sci Ctr, Oxford Rd, Manchester M13 9PT, Lancs, England
Jarnuczak, Andrew F.
Albornoz, Manuel Garcia
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Univ Manchester, Sch Biol Sci, Fac Biol Med & Hlth, Manchester Acad Hlth Sci Ctr, Oxford Rd, Manchester M13 9PT, Lancs, EnglandUniv Manchester, Sch Biol Sci, Fac Biol Med & Hlth, Manchester Acad Hlth Sci Ctr, Oxford Rd, Manchester M13 9PT, Lancs, England
Albornoz, Manuel Garcia
Eyers, Claire E.
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Univ Liverpool, Inst Integrat Biol, Dept Biochem, Ctr Proteome Res, Liverpool L69 7ZB, Merseyside, EnglandUniv Manchester, Sch Biol Sci, Fac Biol Med & Hlth, Manchester Acad Hlth Sci Ctr, Oxford Rd, Manchester M13 9PT, Lancs, England
Eyers, Claire E.
Grant, Christopher M.
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Univ Manchester, Sch Biol Sci, Fac Biol Med & Hlth, Manchester Acad Hlth Sci Ctr, Oxford Rd, Manchester M13 9PT, Lancs, EnglandUniv Manchester, Sch Biol Sci, Fac Biol Med & Hlth, Manchester Acad Hlth Sci Ctr, Oxford Rd, Manchester M13 9PT, Lancs, England
Grant, Christopher M.
Hubbard, Simon J.
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Univ Manchester, Sch Biol Sci, Fac Biol Med & Hlth, Manchester Acad Hlth Sci Ctr, Oxford Rd, Manchester M13 9PT, Lancs, EnglandUniv Manchester, Sch Biol Sci, Fac Biol Med & Hlth, Manchester Acad Hlth Sci Ctr, Oxford Rd, Manchester M13 9PT, Lancs, England