Hughes Hallett James E, Luo Xiangxia, Capaldi Andrew P
Department of Molecular and Cellular Biology, University of Arizona, Tucson, United States.
Elife. 2015 Oct 6;4:e09181. doi: 10.7554/eLife.09181.
The target of rapamycin complex I (TORC1) regulates cell growth and metabolism in eukaryotes. Previous studies have shown that nitrogen and amino acid signals activate TORC1 via the small GTPases, Gtr1/2. However, little is known about the way that other nutrient signals are transmitted to TORC1. Here we report that glucose starvation triggers disassembly of TORC1, and movement of the key TORC1 component Kog1/Raptor to a single body near the edge of the vacuole. These events are driven by Snf1/AMPK-dependent phosphorylation of Kog1 at Ser 491/494 and two nearby prion-like motifs. Kog1-bodies then serve to increase the threshold for TORC1 activation in cells that have been starved for a significant period of time. Together, our data show that Kog1-bodies create hysteresis (memory) in the TORC1 pathway and help ensure that cells remain committed to a quiescent state under suboptimal conditions. We suggest that other protein bodies formed in starvation conditions have a similar function.
雷帕霉素靶蛋白复合体I（TORC1）调控真核生物中的细胞生长和代谢。先前的研究表明，氮和氨基酸信号通过小GTP酶Gtr1/2激活TORC1。然而，对于其他营养信号传递给TORC1的方式却知之甚少。在此我们报告，葡萄糖饥饿会触发TORC1的解体，以及TORC1关键组分Kog1/Raptor向液泡边缘附近的一个单一体移动。这些事件是由Snf1/AMPK依赖的Kog1在丝氨酸491/494以及两个附近的类朊病毒基序处的磷酸化所驱动的。然后，Kog1体在长时间饥饿的细胞中提高了TORC1激活的阈值。总之，我们的数据表明，Kog1体在TORC1途径中产生滞后现象（记忆），并有助于确保细胞在次优条件下保持静止状态。我们认为，在饥饿条件下形成的其他蛋白体具有类似的功能。
