Department of Molecular, Cell, and Developmental Biology, University of California, Santa Cruz, California 95064.
Department of Molecular, Cell, and Developmental Biology, University of California, Santa Cruz, California 95064
Genetics. 2018 Sep;210(1):155-170. doi: 10.1534/genetics.118.301296. Epub 2018 Jul 9.
Nutrient availability, growth rate, and cell size are closely linked. For example, in budding yeast, the rate of cell growth is proportional to nutrient availability, cell size is proportional to growth rate, and growth rate is proportional to cell size. Thus, cells grow slowly in poor nutrients and are nearly half the size of cells growing in rich nutrients. Moreover, large cells grow faster than small cells. A signaling network that surrounds TOR kinase complex 2 (TORC2) plays an important role in enforcing these proportional relationships. Cells that lack components of the TORC2 network fail to modulate their growth rate or size in response to changes in nutrient availability. Here, we show that budding yeast homologs of the Lkb1 tumor suppressor kinase are required for normal modulation of TORC2 signaling in response to changes in carbon source. Lkb1 kinases activate Snf1/AMPK to initiate transcription of genes required for utilization of poor carbon sources. However, Lkb1 influences TORC2 signaling via a novel pathway that is independent of Snf1/AMPK. Of the three Lkb1 homologs in budding yeast, Elm1 plays the most important role in modulating TORC2. Elm1 activates a pair of related kinases called Gin4 and Hsl1. Previous work found that loss of Gin4 and Hsl1 causes cells to undergo unrestrained growth during a prolonged mitotic arrest, which suggests that they play a role in linking cell cycle progression to cell growth. We found that Gin4 and Hsl1 also control the TORC2 network. In addition, Gin4 and Hsl1 are themselves influenced by signals from the TORC2 network, consistent with previous work showing that the TORC2 network constitutes a feedback loop. Together, the data suggest a model in which the TORC2 network sets growth rate in response to carbon source, while also relaying signals via Gin4 and Hsl1 that set the critical amount of growth required for cell cycle progression. This kind of close linkage between control of cell growth and size would suggest a simple mechanistic explanation for the proportional relationship between cell size and growth rate.
养分可用性、生长速率和细胞大小密切相关。例如,在出芽酵母中,细胞生长速率与养分可用性成正比,细胞大小与生长速率成正比,而生长速率又与细胞大小成正比。因此,在营养匮乏的情况下,细胞生长缓慢,其大小只有在营养丰富的情况下生长的细胞的一半。此外,大细胞的生长速度比小细胞快。一个环绕雷帕霉素靶蛋白激酶复合物 2(TORC2)的信号网络在强制实施这些比例关系方面起着重要作用。缺乏 TORC2 网络组件的细胞无法根据养分可用性的变化来调节其生长速率或大小。在这里,我们表明,出芽酵母 Lkb1 肿瘤抑制激酶的同源物对于正常调节 TORC2 信号以响应碳源变化是必需的。Lkb1 激酶激活 Snf1/AMPK 以启动利用贫碳源所需基因的转录。然而,Lkb1 通过一种不依赖于 Snf1/AMPK 的新途径影响 TORC2 信号。在出芽酵母的三个 Lkb1 同源物中,Elm1 在调节 TORC2 方面起着最重要的作用。Elm1 激活一对称为 Gin4 和 Hsl1 的相关激酶。之前的工作发现,Gin4 和 Hsl1 的缺失导致细胞在长时间的有丝分裂停滞期间不受控制地生长,这表明它们在将细胞周期进程与细胞生长联系起来方面发挥作用。我们发现 Gin4 和 Hsl1 也控制 TORC2 网络。此外,Gin4 和 Hsl1 本身也受到来自 TORC2 网络的信号的影响,这与之前的工作一致,表明 TORC2 网络构成一个反馈回路。总之,数据表明,TORC2 网络根据碳源设定生长速率,同时通过 Gin4 和 Hsl1 传递信号,为细胞周期进程设定所需的临界生长量。这种细胞生长和大小控制之间的紧密联系将为细胞大小与生长速率之间的比例关系提供一个简单的机械解释。