PT  - JOURNAL ARTICLE
AU  - Liu, Wei
AU  - Lowrey, Harper
AU  - Leung, Chun Chung
AU  - Adamchek, Christopher
AU  - Du, Juan
AU  - He, Jiangman
AU  - Chen, Meng
AU  - Gendron, Joshua M.
TI  - The circadian clock regulates PIF3 protein stability in parallel to red light
AID  - 10.1101/2023.09.18.558326
DP  - 2023 Jan 01
TA  - bioRxiv
PG  - 2023.09.18.558326
4099  - http://biorxiv.org/content/early/2023/09/18/2023.09.18.558326.short
4100  - http://biorxiv.org/content/early/2023/09/18/2023.09.18.558326.full
AB  - The circadian clock is an endogenous oscillator, but its importance lies in its ability to impart rhythmicity on downstream biological processes or outputs. Focus has been placed on understanding the core transcription factors of the circadian clock and how they connect to outputs through regulated gene transcription. However, far less is known about posttranslational mechanisms that tether clocks to output processes through protein regulation. Here, we identify a protein degradation mechanism that tethers the clock to photomorphogenic growth. By performing a reverse genetic screen, we identify a clock-regulated F-box type E3 ubiquitin ligase, CLOCK-REGULATED F-BOX WITH A LONG HYPOCOTYL 1 (CFH1), that controls hypocotyl length. We then show that CFH1 functions in parallel to red light signaling to target the transcription factor PIF3 for degradation. This work demonstrates that the circadian clock is tethered to photomorphogenesis through the ubiquitin proteasome system and that PIF3 protein stability acts as a hub to integrate information from multiple environmental signals.Competing Interest StatementThe authors have declared no competing interest.