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

核心时钟蛋白的冷诱导降解实现了拟南芥昼夜节律时钟的温度补偿

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作者:Akari E Maeda, Hiromi Matsuo, Tomoaki Muranaka, Norihito Nakamichi

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 Arabidopsis thaliana. The prr5 toc1 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 lkp2 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 LKP2-dependent control of PRR5 and TOC1 abundance.

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