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Phosphorylation of the Transcription Factor Atf1 at Multiple Sites by the MAP Kinase Sty1 Controls Homologous Recombination and Transcription.
J Mol Biol. 2020 09 04; 432(19):5430-5446.JM

Abstract

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.

Authors+Show Affiliations

Oxidative Stress and Cell Cycle Group, Universitat Pompeu Fabra, Barcelona, Spain.Oxidative Stress and Cell Cycle Group, Universitat Pompeu Fabra, Barcelona, Spain.Oxidative Stress and Cell Cycle Group, Universitat Pompeu Fabra, Barcelona, Spain.Oxidative Stress and Cell Cycle Group, Universitat Pompeu Fabra, Barcelona, Spain. Electronic address: elena.hidalgo@upf.edu.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

32795531

Citation

Sánchez-Mir, Laura, et al. "Phosphorylation of the Transcription Factor Atf1 at Multiple Sites By the MAP Kinase Sty1 Controls Homologous Recombination and Transcription." Journal of Molecular Biology, vol. 432, no. 19, 2020, pp. 5430-5446.
Sánchez-Mir L, Fraile R, Ayté J, et al. Phosphorylation of the Transcription Factor Atf1 at Multiple Sites by the MAP Kinase Sty1 Controls Homologous Recombination and Transcription. J Mol Biol. 2020;432(19):5430-5446.
Sánchez-Mir, L., Fraile, R., Ayté, J., & Hidalgo, E. (2020). Phosphorylation of the Transcription Factor Atf1 at Multiple Sites by the MAP Kinase Sty1 Controls Homologous Recombination and Transcription. Journal of Molecular Biology, 432(19), 5430-5446. https://doi.org/10.1016/j.jmb.2020.08.004
Sánchez-Mir L, et al. Phosphorylation of the Transcription Factor Atf1 at Multiple Sites By the MAP Kinase Sty1 Controls Homologous Recombination and Transcription. J Mol Biol. 2020 09 4;432(19):5430-5446. PubMed PMID: 32795531.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Phosphorylation of the Transcription Factor Atf1 at Multiple Sites by the MAP Kinase Sty1 Controls Homologous Recombination and Transcription. AU - Sánchez-Mir,Laura, AU - Fraile,Rodrigo, AU - Ayté,José, AU - Hidalgo,Elena, Y1 - 2020/08/11/ PY - 2020/06/08/received PY - 2020/07/31/revised PY - 2020/08/04/accepted PY - 2020/8/17/pubmed PY - 2021/3/10/medline PY - 2020/8/16/entrez KW - Atf1 KW - Schizosaccharomyces pombe KW - Sty1 KW - homologous recombination KW - transcription regulation SP - 5430 EP - 5446 JF - Journal of molecular biology JO - J Mol Biol VL - 432 IS - 19 N2 - 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. SN - 1089-8638 UR - https://www.unboundmedicine.com/medline/citation/32795531/Phosphorylation_of_the_Transcription_Factor_Atf1_at_Multiple_Sites_by_the_MAP_Kinase_Sty1_Controls_Homologous_Recombination_and_Transcription_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0022-2836(20)30487-3 DB - PRIME DP - Unbound Medicine ER -