Phosphorylation of the Transcription Factor Atf1 at Multiple Sites by the MAP Kinase Sty1 Controls Homologous Recombination and Transcription
| Autor: | Elena Hidalgo, Laura Sánchez-Mir, Rodrigo Fraile, José Ayté |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
Transcriptional Activation
Biology Chromatin remodeling 03 medical and health sciences 0302 clinical medicine Structural Biology Transcription (biology) Gene Expression Regulation Fungal Schizosaccharomyces Atf1 Gene expression Transcriptional regulation Phosphorylation Sty1 Homologous recombination Molecular Biology Transcription factor 030304 developmental biology Activating Transcription Factor 1 0303 health sciences ATF1 Kinase Transcription regulation Chromatin Assembly and Disassembly Phosphoproteins Cell biology Schizosaccharomyces pombe Mutation Schizosaccharomyces pombe Proteins Mitogen-Activated Protein Kinases Protein Processing Post-Translational 030217 neurology & neurosurgery |
| Zdroj: | Journal of Molecular Biology. 432:5430-5446 |
| ISSN: | 0022-2836 |
| DOI: | 10.1016/j.jmb.2020.08.004 |
| Popis: | Transcription factors are often the downstream effectors of signaling cascades. In fission yeast, the transcription factor Atf1 is phosphorylated by the MAP kinase Sty1 under several environmental stressors to promote transcription initiation of stress genes. However, Sty1 and Atf1 have also been involved in other cellular processes such as homologous recombination at hotspots, ste11 gene expression during mating and meiosis, or regulation of fbp1 gene transcription under glucose starvation conditions. Using different phospho-mutants of Atf1, we have investigated the role of Atf1 phosphorylation by Sty1 in those biological processes. An Atf1 mutant lacking the canonical MAP kinase phosphorylation sites cannot activate fbp1 transcription when glucose is depleted, but it is still able to induce recombination at ade6.M26 and to induce ste11 after nitrogen depletion; in these last cases, Sty1 is still required, suggesting that additional non-canonical sites are activating the transcription factor. In all cases, an Atf1 phosphomimetic mutant bypasses the requirement of the Sty1 kinase in these diverse biological processes, highlighting the essential role of the DNA binding factor Atf1 on chromatin remodeling and cell adaptation to nutritional changes. We propose that post-translational modifications of Atf1 by Sty1, either at canonical or non-canonical sites, are sufficient to activate some of the functions of Atf1, those involving chromatin remodeling and transcription initiation. However, in the case of fbp1 where Atf1 acts synergistically with other transcription factors, elimination of the canonical sites is sufficient to hamper some of the interactions required in this complex scenario and to impair transcription initiation. We are thankful to Dr. Masayuki Yamamoto for providing strain JX233. This work is supported by the Ministerio de Ciencia, Innovación y Universidades (Spain), PLAN E and FEDER (PGC2018-093920-B-I00 to E.H.). The Oxidative Stress and Cell Cycle group is also supported by Generalitat de Catalunya (Spain) (2017-SGR-539) and by Unidad de Excelencia María de Maeztu from the Ministerio de Ciencia, Innovación y Universidades (CEX2018-000792-M) (Spain). |
| Databáze: | OpenAIRE |
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