Journal
CURRENT BIOLOGY
Volume 31, Issue 1, Pages 138-+Publisher
CELL PRESS
DOI: 10.1016/j.cub.2020.10.013
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Funding
- NCI CCSG [P30 CA060553, P41 GM108569]
- National Institutes of Health (NIH) [R01NS106955]
- DARPA [D12AP00023]
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This study demonstrates that PRL-1 regulates period length and phase of the clock by promoting TIM dephosphorylation, allowing animals to adjust their behavior to changing day-night cycles.
The timing of behavior under natural light-dark conditions is a function of circadian clocks and photic input pathways, but a mechanistic understanding of how these pathways collaborate in animals is lacking. Here we demonstrate in Drosophila that the Phosphatase of Regenerating Liver-1 (PRL-1) sets period length and behavioral phase gated by photic signals. PRL-1 knockdown in PDF clock neurons dramatically lengthens circadian period. PRL-1 mutants exhibit allele-specific interactions with the light- and clock-regulated gene timeless (tim). Moreover, we show that PRL-1 promotes TIM accumulation and dephosphorylation. Interestingly, the PRL-1 mutant period lengthening is suppressed in constant light, and PRL-1 mutants display a delayed phase under short, but not long, photoperiod conditions. Thus, our studies reveal that PRL-1-dependent dephosphorylation of TIM is a core mechanism of the clock that sets period length and phase in darkness, enabling the behavioral adjustment to change day-night cycles.
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