unfolded 蛋白反应的进化方面。
Evolutionary Aspects of the Unfolded Protein Response.
机构信息
Department of Biophysics, Graduate School of Science, Kyoto University, Kyoto 606-8502, Japan.
出版信息
Cold Spring Harb Perspect Biol. 2022 Dec 1;14(12):a041262. doi: 10.1101/cshperspect.a041262.
Abstract
The unfolded protein response (UPR) is activated when unfolded proteins accumulate in the endoplasmic reticulum (ER). The basic mechanism of the UPR in maintaining ER homeostasis has been clarified from yeast to humans. The UPR is triggered by one or more transmembrane proteins in the ER. The number of canonical UPR sensors/transducers has increased during evolution, from one (IRE1) in yeast to three (IRE1, PERK, and ATF6) in invertebrates and five (IRE1α, IRE1β, PERK, ATF6α, and ATF6β) in vertebrates. Here, I initially describe the four major changes that have occurred during evolution: (1) advent of PERK in metazoans; (2) switch in transcription factor downstream of IRE1 in metazoans; (3) switch in regulator of ER chaperone induction in vertebrates; and (4) increase in the number of ATF6-like local factors in vertebrates. I then discuss the causes of the phenotypes of vertebrate knockout animals and refer to regulated IRE1-dependent decay of mRNAs.
摘要
未折叠蛋白反应（UPR）在折叠蛋白在内质网（ER）中积累时被激活。从酵母到人，已经阐明了 UPR 维持 ER 稳态的基本机制。UPR 是由 ER 中的一种或多种跨膜蛋白触发的。在进化过程中，经典的 UPR 传感器/转导器的数量增加，从酵母中的一个（IRE1）增加到无脊椎动物中的三个（IRE1、PERK 和 ATF6），再增加到脊椎动物中的五个（IRE1α、IRE1β、PERK、ATF6α 和 ATF6β）。在这里，我最初描述了在进化过程中发生的四个主要变化：（1）多细胞动物中 PERK 的出现；（2）多细胞动物中 IRE1 下游转录因子的转变；（3）脊椎动物中 ER 伴侣诱导调节剂的转变；（4）脊椎动物中 ATF6 样局部因子数量的增加。然后，我讨论了脊椎动物基因敲除动物表型的原因，并提到了受调控的 IRE1 依赖性 mRNA 降解。
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