ArticleDevelopmental biology2011
Regulation of the C. elegans molt by pqn-47.
Article in Developmental biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 44 citations in OpenAlex.
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- The NHR-23-regulated putative protease inhibitorbioRxiv : the preprint server for biology · 2024Article
- Essential function of transmembrane transcription factor MYRF in promoting transcription of miRNAeLife · 2024Article
- C. elegans molting requires rhythmic accumulation of the Grainyhead/LSF transcription factor GRH-1.The EMBO journal · 2023Article
- Differential regulation of degradation and immune pathways underlies adaptation of the ectosymbiotic nematode Laxus oneistus to oxic-anoxic interfaces.Scientific reports · 2022Article
- The LRR-TM protein PAN-1 interacts with MYRF to promote its nuclear translocation in synaptic remodeling.eLife · 2021Article
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- Elucidating the transactivation domain of the pleiotropic transcription factor Myrf.Scientific reports · 2018Article
- Building stereotypic connectivity: mechanistic insights into structural plasticity from C. elegans.Current opinion in neurobiology · 2018Review
- Homo-trimerization is essential for the transcription factor function of Myrf for oligodendrocyte differentiation.Nucleic acids research · 2017Article
- Microfluidic platform with spatiotemporally controlled micro-environment for studying long-term C. elegans developmental arrests.Lab on a chip · 2017Article
- Myrf ER-Bound Transcription Factors Drive C. elegans Synaptic Plasticity via Cleavage-Dependent Nuclear Translocation.Developmental cell · 2017Article
- Molting inWorm · 2017Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
C. elegans molts at the end of each of its four larval stages but this cycle ceases at the reproductive adult stage. We have identified a regulator of molting, pqn-47. Null mutations in pqn-47 cause a developmental arrest at the first larval molt, showing that this gene activity is required to transit the molt. Mutants with weak alleles of pqn-47 complete the larval molts but fail to exit the molting cycle at the adult stage. These phenotypes suggest that pqn-47 executes key aspects of the molting program including the cessation of molting cycles. The pqn-47 gene encodes a protein that is highly conserved in animal phylogeny but probably misannotated in genome sequences due to much less significant homology to a yeast transcription factor. A PQN-47::GFP fusion gene is expressed in many neurons, vulval precursor cells, the distal tip cell (DTC), intestine, and the lateral hypodermal seam cells but not in the main body hypodermal syncytium (hyp7) that underlies, synthesizes, and releases most of the collagenous cuticle. A functional PQN-47::GFP fusion protein localizes to the cytoplasm rather than the nucleus at all developmental stages, including the periods preceding and during ecdysis when genetic analysis suggests that pqn-47 functions. The cytoplasmic localization of PQN-47::GFP partially overlaps with the endoplasmic reticulum, suggesting that PQN-47 is involved in the extensive secretion of cuticle components or hormones that occurs during molts. The mammalian and insect homologues of pqn-47 may serve similar roles in regulated secretion.
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Registered trials
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.