ArticleCell reports2021
C. elegans LIN-28 controls temporal cell fate progression by regulating LIN-46 expression via the 5' UTR of lin-46 mRNA.
Article in Cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- let-7 miRNA and lin-46 mRNA are essential targets of the LIN28 RNA-binding protein in Caenorhabditis elegans developmental timing regulation.PLoS biology · 2026Article
- Multi-dimensional regulation of LIN-28 temporal expression dynamics in the C. elegans heterochronic gene cascade.Development (Cambridge, England) · 2026Article
- Somatic gonad morphogenesis in C. elegans requires the heterochronic pathway acting through HBL-1.G3 (Bethesda, Md.) · 2025Article
- A temporal sequence of heterochronic gene activities promotes stage-specific developmental events in Caenorhabditis elegans.G3 (Bethesda, Md.) · 2024Article
- LIN28 upregulation in primary human T cells impaired CAR T antitumoral activity.Frontiers in immunology · 2024Article
- Orthologs of the Caenorhabditis elegans heterochronic genes have divergent functions in Caenorhabditis briggsae.Genetics · 2023Article
- A branched heterochronic pathway directs juvenile-to-adult transition through two LIN-29 isoforms.eLife · 2020Article
- Regulation of nuclear-cytoplasmic partitioning by theDevelopment (Cambridge, England) · 2019Article
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3 authors at 1 institution in 1 country.
Funding
Abstract
Lin28/LIN-28 is a conserved RNA-binding protein that promotes proliferation and pluripotency and can be oncogenic in mammals. Mammalian Lin28 and C. elegans LIN-28 have been shown to inhibit biogenesis of the conserved cellular differentiation-promoting microRNA let-7 by directly binding to unprocessed let-7 transcripts. Lin28/LIN-28 also bind and regulate many mRNAs in diverse cell types. However, the determinants and consequences of LIN-28-mRNA interactions are not well understood. Here, we report that C. elegans LIN-28 represses the expression of LIN-46, a downstream protein in the heterochronic pathway. We find that lin-28 and sequences within the lin-46 5' UTR are required to prevent LIN-46 expression at early larval stages. Moreover, we find that precocious LIN-46 expression caused by mutations in the lin-46 5' UTR is sufficient to cause precocious heterochronic defects similar to those of lin-28(lf) animals. Thus, our findings demonstrate the biological importance of the regulation of individual target mRNAs by LIN-28.
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