ArticleDevelopment (Cambridge, England)2023
NHR-23 activity is necessary for C. elegans developmental progression and apical extracellular matrix structure and function.
Article in Development (Cambridge, England), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 36 citations in OpenAlex.
- Secreted filarial acetylcholine analogs modulate parasite reproduction and host physiology.Nature communications · 2026Article
- Opposing roles for lipocalins and a CD36 family scavenger receptor in apical extracellular matrix-dependent protection of narrow tube integrity.Development (Cambridge, England) · 2026Article
- Multiple losses of ecdysone receptor genes in nematodes: an alternative evolutionary scenario of molting regulation.Molecular biology and evolution · 2026Article
- Roles and regulation of the Kunitz domain protein MLT-11 during C. elegans cuticle synthesis and molting.Genetics · 2026Article
- MYRF drives heterochronic miRNAs and LIN-42, and amplifies oscillatory programs for stage transitions.bioRxiv : the preprint server for biology · 2026Article
- Dual Inhibition of MYRF Cleavage by Its JM Region and PAN-1 CCT Gates Developmental Timing inbioRxiv : the preprint server for biology · 2026Article
- Article
- The interplay betweeniScience · 2025Article
- MLT-11 is necessary forbioRxiv : the preprint server for biology · 2025Article
- A conserved chronobiological complex times C. elegans development.The EMBO journal · 2025Article
- Systematic identification of oscillatory gene expression in single cell types.bioRxiv : the preprint server for biology · 2025Article
- Multiscale patterning of a model apical extracellular matrix revealed by systematic endogenous protein tagging.bioRxiv : the preprint server for biology · 2025Article
- A wrinkle in timers: evolutionary rewiring of conserved biological timekeepers.Trends in biochemical sciences · 2025Review
- TAT-1, a phosphatidylserine flippase, affects molting and regulates membrane trafficking in the epidermis of Caenorhabditis elegans.Genetics · 2025Article
- A defining member of the new cysteine-cradle family is an aECM protein signalling skin damage in C. elegans.PLoS genetics · 2025Article
- Morphologically defined substages of tail morphogenesis in C. elegans males.Developmental dynamics : an official publication of the American Association of Anatomists · 2024Review
- A defining member of the new cysteine-cradle family is an aECM protein signalling skin damage inbioRxiv : the preprint server for biology · 2024Article
- Loss of the Na+/K+ cation pump CATP-1 suppresses nekl-associated molting defects.G3 (Bethesda, Md.) · 2024Article
- The NHR-23-regulated putative protease inhibitorbioRxiv : the preprint server for biology · 2024Article
- Tissue-specific RNA-seq defines genes governing male tail tip morphogenesis in C. elegans.Development (Cambridge, England) · 2024Article
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Nematode molting is a remarkable process where animals must repeatedly build a new apical extracellular matrix (aECM) beneath a previously built aECM that is subsequently shed. The nuclear hormone receptor NHR-23 (also known as NR1F1) is an important regulator of C. elegans molting. NHR-23 expression oscillates in the epidermal epithelium, and soma-specific NHR-23 depletion causes severe developmental delay and death. Tissue-specific RNAi suggests that nhr-23 acts primarily in seam and hypodermal cells. NHR-23 coordinates the expression of factors involved in molting, lipid transport/metabolism and remodeling of the aECM. NHR-23 depletion causes dampened expression of a nas-37 promoter reporter and a loss of reporter oscillation. The cuticle collagen ROL-6 and zona pellucida protein NOAH-1 display aberrant annular localization and severe disorganization over the seam cells after NHR-23 depletion, while the expression of the adult-specific cuticle collagen BLI-1 is diminished and frequently found in patches. Consistent with these localization defects, the cuticle barrier is severely compromised when NHR-23 is depleted. Together, this work provides insight into how NHR-23 acts in the seam and hypodermal cells to coordinate aECM regeneration during development.
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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.