Bandhakavi Sricharan, Xie Hongwei, O'Callaghan Brennon, Sakurai Hiroshi, Kim Do-Hyung, Griffin Timothy J
Department of Biochemistry, Molecular Biology and Biophysics, University of Minnesota, Minneapolis, Minnesota, USA.
PLoS One. 2008 Feb 13;3(2):e1598. doi: 10.1371/journal.pone.0001598.
TOR kinases integrate environmental and nutritional signals to regulate cell growth in eukaryotic organisms. Here, we describe results from a study combining quantitative proteomics and comparative expression analysis in the budding yeast, S. cerevisiae, to gain insights into TOR function and regulation. We profiled protein abundance changes under conditions of TOR inhibition by rapamycin treatment, and compared this data to existing expression information for corresponding gene products measured under a variety of conditions in yeast. Among proteins showing abundance changes upon rapamycin treatment, almost 90% of them demonstrated homodirectional (i.e., in similar direction) transcriptomic changes under conditions of heat/oxidative stress. Because the known downstream responses regulated by Tor1/2 did not fully explain the extent of overlap between these two conditions, we tested for novel connections between the major regulators of heat/oxidative stress response and the TOR pathway. Specifically, we hypothesized that activation of regulator(s) of heat/oxidative stress responses phenocopied TOR inhibition and sought to identify these putative TOR inhibitor(s). Among the stress regulators tested, we found that cells (hsf1-R206S, F256S and ssa1-3 ssa2-2) constitutively activated for heat shock transcription factor 1, Hsf1, inhibited rapamycin resistance. Further analysis of the hsf1-R206S, F256S allele revealed that these cells also displayed multiple phenotypes consistent with reduced TOR signaling. Among the multiple Hsf1 targets elevated in hsf1-R206S, F256S cells, deletion of PIR3 and YRO2 suppressed the TOR-regulated phenotypes. In contrast to our observations in cells activated for Hsf1, constitutive activation of other regulators of heat/oxidative stress responses, such as Msn2/4 and Hyr1, did not inhibit TOR signaling. Thus, we propose that activated Hsf1 inhibits rapamycin resistance and TOR signaling via elevated expression of specific target genes in S. cerevisiae. Additionally, these results highlight the value of comparative expression analyses between large-scale proteomic and transcriptomic datasets to reveal new regulatory connections.
TOR激酶整合环境和营养信号以调控真核生物中的细胞生长。在此,我们描述了一项结合定量蛋白质组学和比较表达分析的研究结果,该研究以芽殖酵母酿酒酵母为对象,旨在深入了解TOR的功能和调控机制。我们分析了雷帕霉素处理抑制TOR条件下蛋白质丰度的变化,并将此数据与酵母在多种条件下测量的相应基因产物的现有表达信息进行比较。在雷帕霉素处理后显示丰度变化的蛋白质中,近90%在热/氧化应激条件下表现出同向(即相似方向)的转录组变化。由于已知由Tor1/2调控的下游反应无法完全解释这两种条件之间的重叠程度,我们测试了热/氧化应激反应的主要调节因子与TOR途径之间的新联系。具体而言,我们假设热/氧化应激反应调节因子的激活模拟了TOR抑制,并试图鉴定这些假定的TOR抑制剂。在测试的应激调节因子中,我们发现持续激活热休克转录因子1(Hsf1)的细胞(hsf1-R206S、F256S和ssa1-3 ssa2-2)抑制了雷帕霉素抗性。对hsf1-R206S、F256S等位基因的进一步分析表明,这些细胞还表现出与TOR信号传导降低一致的多种表型。在hsf1-R206S、F256S细胞中升高的多个Hsf1靶标中,删除PIR3和YRO2可抑制TOR调控的表型。与我们在激活Hsf1的细胞中的观察结果相反,热/氧化应激反应的其他调节因子(如Msn2/4和Hyr1)的持续激活并未抑制TOR信号传导。因此,我们提出激活的Hsf1通过酿酒酵母中特定靶基因的表达升高来抑制雷帕霉素抗性和TOR信号传导。此外,这些结果突出了大规模蛋白质组学和转录组学数据集之间比较表达分析在揭示新调控联系方面的价值。