RCB initiates Arabidopsis thermomorphogenesis by stabilizing the thermoregulator PIF4 in the daytime

Yongjian Qiu (), Elise K. Pasoreck, Chan Yul Yoo, Jiangman He, He Wang, Abhishesh Bajracharya, Meina Li, Haley D. Larsen, Stacey Cheung and Meng Chen ()
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Yongjian Qiu: University of California
Elise K. Pasoreck: University of California
Chan Yul Yoo: University of California
Jiangman He: University of California
He Wang: University of California
Abhishesh Bajracharya: University of Mississippi
Meina Li: University of California
Haley D. Larsen: University of California
Stacey Cheung: University of California
Meng Chen: University of California

Nature Communications, 2021, vol. 12, issue 1, 1-13

Abstract: Abstract Daytime warm temperature elicits thermomorphogenesis in Arabidopsis by stabilizing the central thermoregulator PHYTOCHROME INTERACTING transcription FACTOR 4 (PIF4), whose degradation is otherwise promoted by the photoreceptor and thermosensor phytochrome B. PIF4 stabilization in the light requires a transcriptional activator, HEMERA (HMR), and is abrogated when HMR’s transactivation activity is impaired in hmr-22. Here, we report the identification of a hmr-22 suppressor mutant, rcb-101, which surprisingly carries an A275V mutation in REGULATOR OF CHLOROPLAST BIOGENESIS (RCB). rcb-101/hmr-22 restores thermoresponsive PIF4 accumulation and reverts the defects of hmr-22 in chloroplast biogenesis and photomorphogenesis. Strikingly, similar to hmr, the null rcb-10 mutant impedes PIF4 accumulation and thereby loses the warm-temperature response. rcb-101 rescues hmr-22 in an allele-specific manner. Consistently, RCB interacts directly with HMR. Together, these results unveil RCB as a novel temperature signaling component that functions collaboratively with HMR to initiate thermomorphogenesis by selectively stabilizing PIF4 in the daytime.

Date: 2021
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DOI: 10.1038/s41467-021-22313-x

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