The Phospho-Code Determining Circadian Feedback Loop Closure and Output in Neurospora.


Journal

Molecular cell
ISSN: 1097-4164
Titre abrégé: Mol Cell
Pays: United States
ID NLM: 9802571

Informations de publication

Date de publication:
16 05 2019
Historique:
received: 14 09 2018
revised: 07 01 2019
accepted: 01 03 2019
pubmed: 8 4 2019
medline: 17 10 2019
entrez: 8 4 2019
Statut: ppublish

Résumé

In the negative feedback loop driving fungal and animal circadian oscillators, negative elements (FREQUENCY [FRQ], PERIODS [PERs], and CRYPTOCHROMES [CRYs]) are understood to inhibit their own expression, in part by promoting the phosphorylation of their heterodimeric transcriptional activators (e.g., White Collar-1 [WC-1]-WC-2 [White Collar complex; WCC] and BMAL1/Circadian Locomotor Output Cycles Kaput [CLOCK]). However, correlations between heterodimer activity and phosphorylation are weak, contradictions exist, and mechanistic details are almost wholly lacking. We report mapping of 80 phosphosites on WC-1 and 15 on WC-2 and elucidation of the time-of-day-specific code, requiring both a group of phosphoevents on WC-1 and two distinct clusters on WC-2, that governs circadian repression, leading to feedback loop closure. Combinatorial control via phosphorylation also governs rhythmic WCC binding to the promoters of clock-controlled genes mediating the essential first step in circadian output, a group encoding both transcription factors and signaling proteins. These data provide a basic mechanistic understanding for fundamental events underlying circadian negative feedback and output, key aspects of circadian biology.

Identifiants

pubmed: 30954403
pii: S1097-2765(19)30177-7
doi: 10.1016/j.molcel.2019.03.003
pmc: PMC6583785
mid: NIHMS1525557
pii:
doi:

Substances chimiques

ARNTL Transcription Factors 0
DNA-Binding Proteins 0
Fungal Proteins 0
Transcription Factors 0
wc-1 protein, Neurospora crassa 0
white collar 2 protein, Neurospora 0

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

771-784.e3

Subventions

Organisme : NIGMS NIH HHS
ID : R35 GM118021
Pays : United States
Organisme : NIGMS NIH HHS
ID : R35 GM118022
Pays : United States
Organisme : NIGMS NIH HHS
ID : R35 GM119455
Pays : United States
Organisme : NIH HHS
ID : S10 OD016212
Pays : United States

Informations de copyright

Copyright © 2019 Elsevier Inc. All rights reserved.

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Auteurs

Bin Wang (B)

Department of Molecular and Systems Biology, Geisel School of Medicine at Dartmouth, Hanover, NH 03755, USA.

Arminja N Kettenbach (AN)

Norris Cotton Cancer Center, Geisel School of Medicine at Dartmouth, Hanover, NH 03755, USA; Department of Biochemistry and Cell Biology, Geisel School of Medicine at Dartmouth, Hanover, NH 03755, USA.

Xiaoying Zhou (X)

Department of Molecular and Systems Biology, Geisel School of Medicine at Dartmouth, Hanover, NH 03755, USA.

Jennifer J Loros (JJ)

Department of Molecular and Systems Biology, Geisel School of Medicine at Dartmouth, Hanover, NH 03755, USA; Department of Biochemistry and Cell Biology, Geisel School of Medicine at Dartmouth, Hanover, NH 03755, USA.

Jay C Dunlap (JC)

Department of Molecular and Systems Biology, Geisel School of Medicine at Dartmouth, Hanover, NH 03755, USA. Electronic address: jay.c.dunlap@dartmouth.edu.

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Classifications MeSH