Differential regulation of transcription: Repression by unactivated mitogen-activated protein kinase Kss1 requires the Dig1 and Dig2 proteins
Differential regulation of transcription: Repression by unactivated mitogen-activated protein kinase Kss1 requires the Dig1 and Dig2 proteins
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DOI：
10.1073/pnas.95.26.15400
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发表时间：
1998-12-22
影响因子：
11.1
通讯作者：
Thorner, J
中科院分区：
文献类型：
--
作者：
Bardwell, L;Cook, JG;Thorner, J
Kss1 是一种酵母丝裂原激活蛋白激酶 (MAPK)，在未磷酸化（未激活）状态下直接结合并抑制 Ste12，Ste12 是启动子含有丝状响应元件 (FRE) 的基因和启动子含有信息素响应元件 (PRE) 的基因表达所必需的转录因子。在此，我们证明了两种核蛋白 Dig1 和 Dig2 是 Kss1 施加的抑制所需的辅助因子。 Dig1 和 Dig2 与 Kss1 合作抑制 Ste12 在 FRE 上的作用并调节自然侵入菌株的侵入生长。 Kss1 强加的 Dig 依赖性 Ste12 抑制也发生在 PRE 处。然而，与 FRE 抑制相比，PRE 抑制的维持更依赖于 Dig1 和/或 Dig2，而较少依赖于 Kss1。此外，PRE 的去抑制比 FRE 的去抑制更依赖于 MAPK 介导的磷酸化。两种类型的 MAPK 介导的调节（结合强加的抑制和磷酸化依赖性激活）的差异利用，与不同的含 Ste12 的复合物相结合，有助于使用相同 MAPK 级联的单独细胞外刺激可以引发两种不同的转录反应的机制。
Kss1, a yeast mitogen-activated protein kinase (MAPK), in its unphosphorylated (unactivated) state binds directly to and represses Ste12, a transcription factor necessary for expression of genes whose promoters contain filamentous response elements (FREs) and genes whose promoters contain pheromone response elements (PREs). Herein we show that two nuclear proteins, Dig1 and Dig2, are required cofactors in Kss1-imposed repression. Dig1 and Dig2 cooperate with Kss1 to repress Ste12 action at FREs and regulate invasive growth in a naturally invasive strain. Kss1-imposed Dig-dependent repression of Ste12 also occurs at PREs. However, maintenance of repression at PREs is more dependent on Dig1 and/or Dig2 and less dependent on Kss1 than repression at FREs. In addition, derepression at PREs is more dependent on MAPK-mediated phosphorylation than is derepression at FREs. Differential utilization of two types of MAPK-mediated regulation (binding-imposed repression and phosphorylation-dependent activation), in combination with distinct Ste12-containing complexes, contributes to the mechanisms by which separate extracellular stimuli that use the same MAPK cascade can elicit two different transcriptional responses.