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.

转录因子通常是信号级联反应的下游效应子。在裂变酵母中，转录因子Atf1在几种环境胁迫下被MAP激酶Sty1磷酸化，以促进胁迫基因的转录起始。但是，Sty1和Atf1也参与了其他细胞过程，例如热点的同源重组，交配和减数分裂过程中ste11基因的表达或葡萄糖饥饿条件下fbp1基因转录的调控。我们使用不同的Atf1磷酸突变体，研究了Sty1在这些生物过程中Atf1磷酸化的作用。缺少规范的MAP激酶磷酸化位点的Atf1突变体不能激活fbp1葡萄糖耗尽时转录，但仍然能够在ade6.M26处诱导重组，并在氮耗尽后诱导ste11；在这些最后的情况下，仍然需要Sty1，这表明其他非规范位点正在激活转录因子。在所有情况下，Atf1拟磷酸酶突变体在这些多样的生物过程中都绕过了Sty1激酶的需求，突出了DNA结合因子Atf1在染色质重塑和细胞适应营养变化方面的重要作用。我们建议由Sty1在标准或非标准位点的Atf1的翻译后修饰足以激活Atf1的某些功能，这些功能涉及染色质重塑和转录起始。但是，在fbp1，其中Atf1与其他转录因子协同作用，消除典型位点足以阻碍这种复杂情况下所需的某些相互作用并损害转录起始。