Inappropriate translation inhibition and P-body formation cause cold-sensitivity in tryptophan-auxotroph yeast mutants
In response to different adverse conditions, most eukaryotic organisms, including Saccharomyces cerevisiae, downregulate protein synthesis through the phosphorylation of eIF2α (eukaryotic initiation factor 2α) by Gcn2, a highly conserved protein kinase. Gcn2 also controls the translation of Gcn4, a transcription factor involved in the induction of amino acid biosynthesis enzymes. Here, we have studied the functional role of Gcn2 and Gcn2-regulating proteins, in controlling translation during temperature downshifts of TRP1 and trp1 yeast cells. Our results suggest that neither cold-instigated amino acid limitation nor Gcn2 are involved in the translation suppression at low temperature. However, loss of TRP1 causes increased eIF2α phosphorylation, Gcn2-dependent polysome disassembly and overactivity of Gcn4, which result in cold-sensitivity. Indeed, knock-out of GCN2 improves cold growth of trp1 cells. Likewise, mutation of several Gcn2-regulators and effectors results in cold-growth effects. Remarkably, we found that Hog1, the osmoresponsive MAPK, plays a role in the regulatory mechanism of Gcn2-eIF2α. Finally, we demonstrated that P-body formation responds to a downshift in temperature in a TRP1-dependent manner and is required for cold tolerance.
| Main Authors: | , , , , , |
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| Other Authors: | |
| Format: | artículo biblioteca |
| Language: | English |
| Published: |
Elsevier
2016-11-15
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| Subjects: | Yeast, Low temperature, Polysomes, Gcn2 pathway, eIF2α, Hog1, Snf1, |
| Online Access: | http://hdl.handle.net/10261/141662 http://dx.doi.org/10.13039/501100003329 http://dx.doi.org/10.13039/501100003359 |
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