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冷诱导核心时钟蛋白的降解在生物钟中实现了温度补偿。

Cold-induced degradation of core clock proteins implements temperature compensation in the circadian clock.

机构信息

Graduate School of Bioagricultural Sciences, Nagoya University, Furo-cho, Chikusa, Nagoya 464-8601, Japan.

出版信息

Sci Adv. 2024 Sep 27;10(39):eadq0187. doi: 10.1126/sciadv.adq0187.

DOI:10.1126/sciadv.adq0187
PMID:39331704
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11430399/
Abstract

The period of circadian clocks is maintained at close to 24 hours over a broad range of physiological temperatures due to temperature compensation of period length. Here, we show that the quantitative control of the core clock proteins TIMING OF CAB EXPRESSION 1 [TOC1; also known as PSEUDO-RESPONSE REGULATOR 1 (PRR1)] and PRR5 is crucial for temperature compensation in . The double mutant has a shortened period at higher temperatures, resulting in weak temperature compensation. Low ambient temperature reduces amounts of PRR5 and TOC1. In low-temperature conditions, PRR5 and TOC1 interact with LOV KELCH PROTEIN 2 (LKP2), a component of the E3 ubiquitin ligase Skp, Cullin, F-box (SCF) complex. The mutations attenuate low temperature-induced decrease of PRR5 and TOC1, and the mutants display longer period only at lower temperatures. Our findings reveal that the circadian clock maintains its period length despite ambient temperature fluctuations through temperature- and -dependent control of PRR5 and TOC1 abundance.

摘要

由于周期长度的温度补偿,生物钟的周期在很宽的生理温度范围内接近 24 小时。在这里,我们表明核心时钟蛋白 TIMING OF CAB EXPRESSION 1 [TOC1;也称为 PSEUDO-RESPONSE REGULATOR 1 (PRR1)] 和 PRR5 的定量控制对于 在温度补偿中至关重要。双突变体在较高温度下周期缩短,导致温度补偿减弱。较低的环境温度会降低 PRR5 和 TOC1 的含量。在低温条件下,PRR5 和 TOC1 与 LOV KELCH PROTEIN 2(LKP2)相互作用,后者是 E3 泛素连接酶 Skp、Cullin、F-box(SCF)复合物的一个组成部分。突变削弱了低温诱导的 PRR5 和 TOC1 的减少,而突变体仅在较低温度下显示出较长的周期。我们的发现表明,生物钟通过 PRR5 和 TOC1 丰度的温度和依赖性控制,尽管环境温度波动,仍能维持其周期长度。

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