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截然不同的TORC1信号分支调节Adc17蛋白酶组合的伴侣表达.

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  • 1MRC-PPU, University of Dundee, Dundee DD1 5EH, UK.

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在酵母细胞中抑制TORC1通过激活细胞壁完整性通路来增加蛋白酶组合,并且需要抑制S6激酶Sch9. 这增强了细胞对压力的适应.

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动氨酸细胞骨 动氨酸细胞骨Mpk1 激酶酶是什么蛋白质酶组合的陪伴者这就是Slt2激酶.这是TORC1信号.

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科学领域:

  • 细胞生物学 细胞生物学
  • 分子生物学分子生物学
  • 生物化学 生物化学

背景情况:

  • 细胞在压力下需要蛋白质适应蛋白质稳态,需要增加蛋白质组合.
  • 蛋白质体组合取决于特定的陪伴者的产生,由复杂的信号网络来调节.

研究的目的:

  • 为了研究调节蛋白酶组合的信号通路,在Saccharomyces cerevisiae中监护人生产.
  • 阐明TORC1抑制和下游效应因子在细胞应激反应和蛋白酶体生物发生中的作用.

主要方法:

  • 抑制拉巴胺素复合物1 (TORC1) 激酶的目标.
  • 分析线粒激活蛋白激酶 (MAPK) Mpk1激活和mRNA重新定位的分析.
  • 通过传感器蛋白 (Wsc1,Wsc3,Wsc4) 和S6激酶Sch9抑制激活细胞壁完整性通路的研究.

主要成果:

  • 在酵母中抑制TORC1激活了细胞壁完整性通路,导致蛋白质酶组合伴侣翻译的增加.
  • 这个过程涉及Mpk1激活和mRNA重新定位到actin补丁.
  • 同时抑制S6激酶Sch9对于驱动蛋白质表达至关重要,表明细胞壁信号之外的双重要求.

结论:

  • 抑制TORC1通过细胞壁完整性信号触发蛋白酶组合的上调,并要求同时抑制Sch9.
  • 这项研究揭示了一种新的信号机制,协调细胞应激适应和蛋白质体生物发生.
  • 这些发现扩大了对调控蛋白质酶组合伴侣生产的调控途径的理解.