ArticleThe EMBO journal2025
A conserved chronobiological complex times C. elegans development.
Article in The EMBO journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
10 citing papers in PubMed.
- A circadian clock gene homolog regulates developmental timing and male mating circuitry iniScience · 2026Article
- A desynchrony mechanism between events triggers a compensatory delay during Caenorhabditis elegans development.PLoS biology · 2026Article
- Multiple losses of ecdysone receptor genes in nematodes: an alternative evolutionary scenario of molting regulation.Molecular biology and evolution · 2026Article
- Desynchrony between events triggers a compensatory delay duringbioRxiv : the preprint server for biology · 2026Article
- Roles and regulation of the Kunitz domain protein MLT-11 during C. elegans cuticle synthesis and molting.Genetics · 2026Article
- MLT-11 is necessary forbioRxiv : the preprint server for biology · 2025Article
- Old cogs, new clocks: a conserved protein complex controls developmental and circadian timing.The EMBO journal · 2025Article
- Systematic identification of oscillatory gene expression in single cell types.bioRxiv : the preprint server for biology · 2025Article
- FLYWCH transcription factors act in a LIN-42/Period autoregulatory loop during gonad migration inbioRxiv : the preprint server for biology · 2025Article
- A wrinkle in timers: evolutionary rewiring of conserved biological timekeepers.Trends in biochemical sciences · 2025Review
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Authors and funding
13 authors.
Funding
Abstract
The mammalian protein PERIOD (PER) and its C. elegans orthologue LIN-42 have been proposed to constitute an evolutionary link between two distinct, circadian and developmental, timing systems. While the function of PER in animal circadian rhythms is well understood molecularly and mechanistically, this is not true for LIN-42's function in timing rhythmic development, reflected in C. elegans molting cycles. We observed arrhythmic molts upon combined deletion of a region comprising two distinct sequence elements previously termed SYQ and LT. This region functions as a casein kinase I (CK1)-binding domain (CK1BD) mediating stable binding to KIN-20, the C. elegans CK1δ/ε orthologue. CK1 phosphorylates LIN-42, and the CK1BD sub-domains SYQ/CKBD-A and LT/CKBD-B play distinct roles in controlling CK1-binding and kinase activity in vitro. KIN-20 and the LIN-42 CK1BD are required for proper molt timing in vivo, and loss of LIN-42 binding or of the phosphorylated LIN-42 tail impairs nuclear accumulation of KIN-20. These findings indicate that LIN-42/PER and KIN-20/CK1 form a functionally conserved signaling module of two distinct chronobiological systems.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.