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Role of Fission Yeast Tup1-like Repressors and Prr1 Transcription Factor in Response to Salt Stress

机译:裂变酵母Tup1样阻遏物和Prr1转录因子在盐胁迫响应中的作用。

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摘要

In Schizosaccharomyces pombe, the Sty1 mitogen-activated protein kinase and the Atf1 transcription factor control transcriptional induction in response to elevated salt concentrations. Herein, we demonstrate that two repressors, Tup11 and Tup12, and the Prr1 transcription factor also function in the response to salt shock. We find that deletion of both tup genes together results in hypersensitivity to elevated cation concentrations (K+ and Ca2+) and we identify cta3+, which encodes an intracellular cation transporter, as a novel stress gene whose expression is positively controlled by the Sty1 pathway and negatively regulated by Tup repressors. The expression of cta3+ is maintained at low levels by the Tup repressors, and relief from repression requires the Sty1, Atf1, and Prr1. Prr1 is also required for KCl-mediated induction of several other Sty1-dependent genes such as gpx1+ and ctt1+. Surprisingly, the KCl-mediated induction of cta3+ expression occurs independently of Sty1 in a tup11Δ tup12Δ mutant and so the Tup repressors link induction to the Sty1 pathway. We also report that in contrast to a number of other Sty1- and Atf1-dependent genes, the expression of cta3+ is induced only by high salt concentrations. However, in the absence of the Tup repressors this specificity is lost and a range of stresses induces cta3+ expression.
机译:在粟酒裂殖酵母中,Sty1丝裂原激活的蛋白激酶和Atf1转录因子响应盐浓度升高来控制转录诱导。在这里,我们证明了两个阻遏物,Tup11和Tup12,以及Prr1转录因子在对盐激反应中也起作用。我们发现两个tup基因的缺失共同导致对升高的阳离子浓度(K +和Ca2 +)过敏,并且我们将编码胞内阳离子转运蛋白的cta3 +识别为一种新型应激基因,其表达受到Sty1途径正调控而受到负调控由Tup压制器。 Tup阻遏物可将cta3 +的表达维持在较低水平,而抑制表达需要Sty1,Atf1和Prr1。 KCl介导的其他几个Sty1依赖性基因(例如gpx1 +和ctt1 +)的诱导也需要Prr1。令人惊讶的是,在tup11Δtup12Δ突变体中,KCl介导的对cta3 +表达的诱导独立于Sty1发生,因此Tup阻遏物将诱导与Sty1途径联系起来。我们还报告说,与许多其他Sty1和Atf1依赖基因相反,cta3 +的表达仅由高盐浓度诱导。但是,在没有Tup阻遏物的情况下,这种特异性会丧失,并且一系列压力会诱导cta3 +表达。

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