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Saccharomyces cerevisiae genes involved in survival of heat shock.

Jarolim S, Ayer A, Pillay B, Gee AC, Phrakaysone A, Perrone GG, Breitenbach M, Dawes IW - G3 (Bethesda) (2013)

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Division of Genetics, Department of Cell Biology, University of Salzburg, Salzburg, A-5020 Austria.

ABSTRACT
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°. 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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Related in: MedlinePlus

Tryptophan starvation induces the heat-shock response. Cells of the BY4741 wild-type and trp5 mutant were grown overnight at 30° in SD medium containing auxotrophic requirements and 10 μM l-tryptophan (which leads to starvation for tryptophan) or 100 μM l-tryptophan (which is in excess). Heat-shock resistance for each culture was determined as indicated in the Materials and Methods.
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fig5: Tryptophan starvation induces the heat-shock response. Cells of the BY4741 wild-type and trp5 mutant were grown overnight at 30° in SD medium containing auxotrophic requirements and 10 μM l-tryptophan (which leads to starvation for tryptophan) or 100 μM l-tryptophan (which is in excess). Heat-shock resistance for each culture was determined as indicated in the Materials and Methods.

Mentions: To verify that l-tryptophan depletion affects heat-shock survival, the heat resistances of the trp5Δ mutant and wild type were determined for cells grown to starvation in defined (SD) medium with a range of concentrations of added l-tryptophan. In cells starved for tryptophan, there was a substantial increase in heat-shock resistance; when tryptophan was present in excess, there was no difference between the mutant and the wild type (Figure 5). This finding raises the question of why the trp deletants are heat-shock resistant in YEPD medium. One possible explanation is that tryptophan is heat labile and present in relatively low concentrations in YEPD, and hence the mutants were probably depleted for tryptophan under the conditions used in the screen. Amino acid analysis of YEPD medium used indicated that the concentration of free tryptophan was very low (<125 nM; 26 μg/mL). One possibility is that under tryptophan limitation the cells may activate the target of rapamycin (TOR) pathway, which is a critical event in the heat-shock response as indicated below.


Saccharomyces cerevisiae genes involved in survival of heat shock.

Jarolim S, Ayer A, Pillay B, Gee AC, Phrakaysone A, Perrone GG, Breitenbach M, Dawes IW - G3 (Bethesda) (2013)

Tryptophan starvation induces the heat-shock response. Cells of the BY4741 wild-type and trp5 mutant were grown overnight at 30° in SD medium containing auxotrophic requirements and 10 μM l-tryptophan (which leads to starvation for tryptophan) or 100 μM l-tryptophan (which is in excess). Heat-shock resistance for each culture was determined as indicated in the Materials and Methods.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3852394&req=5

fig5: Tryptophan starvation induces the heat-shock response. Cells of the BY4741 wild-type and trp5 mutant were grown overnight at 30° in SD medium containing auxotrophic requirements and 10 μM l-tryptophan (which leads to starvation for tryptophan) or 100 μM l-tryptophan (which is in excess). Heat-shock resistance for each culture was determined as indicated in the Materials and Methods.
Mentions: To verify that l-tryptophan depletion affects heat-shock survival, the heat resistances of the trp5Δ mutant and wild type were determined for cells grown to starvation in defined (SD) medium with a range of concentrations of added l-tryptophan. In cells starved for tryptophan, there was a substantial increase in heat-shock resistance; when tryptophan was present in excess, there was no difference between the mutant and the wild type (Figure 5). This finding raises the question of why the trp deletants are heat-shock resistant in YEPD medium. One possible explanation is that tryptophan is heat labile and present in relatively low concentrations in YEPD, and hence the mutants were probably depleted for tryptophan under the conditions used in the screen. Amino acid analysis of YEPD medium used indicated that the concentration of free tryptophan was very low (<125 nM; 26 μg/mL). One possibility is that under tryptophan limitation the cells may activate the target of rapamycin (TOR) pathway, which is a critical event in the heat-shock response as indicated below.

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Division of Genetics, Department of Cell Biology, University of Salzburg, Salzburg, A-5020 Austria.

ABSTRACT
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°. 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.

Show MeSH
Related in: MedlinePlus