ArticlePloS one2012
A directed RNAi screen based on larval growth arrest reveals new modifiers of C. elegans insulin signaling.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- ThemicroPublication biology · 2026Article
- A proinsulin-dependent interaction between ENPL-1 and ASNA-1 in neurons is required to maintain insulin secretion in C. elegans.Development (Cambridge, England) · 2023Article
- An antisteatosis response regulated by oleic acid through lipid droplet-mediated ERAD enhancement.Science advances · 2023Article
- Alternative redox forms of ASNA-1 separate insulin signaling from tail-anchored protein targeting and cisplatin resistance in C. elegans.Scientific reports · 2021Article
- ENPL-1, theDevelopment (Cambridge, England) · 2020Article
- A quantitative genome-wide RNAi screen in C. elegans for antifungal innate immunity genes.BMC biology · 2016Article
- Diapause is associated with a change in the polarity of secretion of insulin-like peptides.Nature communications · 2016Article
- To grow or not to grow: nutritional control of development during Caenorhabditis elegans L1 arrest.Genetics · 2013Review
- Depletion of the ER chaperone ENPL-1 sensitizes C. elegans to the anticancer drug cisplatin.Worm · 2013Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genes regulating Caenorhabditis elegans insulin/IGF signaling (IIS) have largely been identified on the basis of their involvement in dauer development or longevity. A third IIS phenotype is the first larval stage (L1) diapause, which is also influenced by asna-1, a regulator of DAF-28/insulin secretion. We reasoned that new regulators of IIS strength might be identified in screens based on the L1 diapause and the asna-1 phenotype. Eighty- six genes were selected for analysis by virtue of their predicted interaction with ASNA-1 and screened for asna-1-like larval arrest. ykt-6, mrps-2, mrps-10 and mrpl-43 were identified as genes which, when inactivated, caused larval arrest without any associated feeding defects. Several tests indicated that IIS strength was weaker and that insulin secretion was defective in these animals. This study highlights the role of the Golgi network and the mitochondria in insulin secretion and provides a new list of genes that modulate IIS in C. elegans.
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