Phosphatase of Regenerating Liver-1 Selectively Times Circadian Behavior in Darkness via Function in PDF Neurons and Dephosphorylation of TIMELESS.


Journal

Current biology : CB
ISSN: 1879-0445
Titre abrégé: Curr Biol
Pays: England
ID NLM: 9107782

Informations de publication

Date de publication:
11 01 2021
Historique:
received: 13 03 2020
revised: 25 08 2020
accepted: 07 10 2020
pubmed: 7 11 2020
medline: 1 9 2021
entrez: 6 11 2020
Statut: ppublish

Résumé

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.

Identifiants

pubmed: 33157022
pii: S0960-9822(20)31517-7
doi: 10.1016/j.cub.2020.10.013
pmc: PMC7855481
mid: NIHMS1638972
pii:
doi:

Substances chimiques

Drosophila Proteins 0
Neuropeptides 0
pdf protein, Drosophila 0
tim protein, Drosophila 0
PRL-1 protein, Drosophila EC 3.1.3.48
Protein Tyrosine Phosphatases EC 3.1.3.48

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, U.S. Gov't, Non-P.H.S.

Langues

eng

Sous-ensembles de citation

IM

Pagination

138-149.e5

Subventions

Organisme : NINDS NIH HHS
ID : R01 NS106955
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK090625
Pays : United States
Organisme : NIGMS NIH HHS
ID : P41 GM108569
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA060553
Pays : United States
Organisme : NHLBI NIH HHS
ID : T32 HL007909
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK113011
Pays : United States
Organisme : NIA NIH HHS
ID : R01 AG065988
Pays : United States
Organisme : NIA NIH HHS
ID : P01 AG011412
Pays : United States

Informations de copyright

Copyright © 2020 Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Interest The authors declare no competing interests.

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Auteurs

Elżbieta Kula-Eversole (E)

Department of Neurobiology, Northwestern University, Evanston, IL 60208, USA.

Da Hyun Lee (DH)

Department of Neurobiology, Northwestern University, Evanston, IL 60208, USA.

Ima Samba (I)

Department of Neurobiology, Northwestern University, Evanston, IL 60208, USA.

Evrim Yildirim (E)

Department of Neurobiology, Northwestern University, Evanston, IL 60208, USA.

Daniel C Levine (DC)

Department of Medicine, Northwestern University, Chicago, IL 60611, USA.

Hee-Kyung Hong (HK)

Department of Medicine, Northwestern University, Chicago, IL 60611, USA.

Bridget C Lear (BC)

Department of Neurobiology, Northwestern University, Evanston, IL 60208, USA.

Joseph Bass (J)

Department of Medicine, Northwestern University, Chicago, IL 60611, USA.

Michael Rosbash (M)

Howard Hughes Medical Institute, Department of Biology, Brandeis University, Waltham, MA 02445, USA.

Ravi Allada (R)

Department of Neurobiology, Northwestern University, Evanston, IL 60208, USA. Electronic address: r-allada@northwestern.edu.

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