ArticleBMC developmental biology2019
Role of PRY-1/Axin in heterochronic miRNA-mediated seam cell development.
Article in BMC developmental biology, 2019. 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, 14 citations in OpenAlex.
- EFL-3/E2F7 modulates Wnt signalling by repressing the Nemo-like kinase LIT-1 during asymmetric epidermal cell division in Caenorhabditis elegans.Development (Cambridge, England) · 2025Article
- Article
- Genetic analysis of Caenorhabditis elegans pry-1/Axin suppressors identifies genes involved in reproductive structure development, stress responses, and aging.G3 (Bethesda, Md.) · 2022Article
- The FGFR4 Homolog KIN-9 Regulates Lifespan and Stress Responses inFrontiers in aging · 2022Article
- AXIN-AMPK signaling: Implications for healthy aging.F1000Research · 2021Review
- Axin-Mediated Regulation of Lifespan and Muscle Health iniScience · 2020Article
- The multifaceted roles of microRNAs in differentiation.Current opinion in cell biology · 2020Review
- Vitellogenin-2 acts downstream of PRY-1/Axin to regulate lipids and lifespan inmicroPublication biology · 2020Article
- Axin Family of Scaffolding Proteins in Development: Lessons fromJournal of developmental biology · 2019Review
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundCaenorhabditis elegans seam cells serve as a good model to understand how genes and signaling pathways interact to control asymmetric cell fates. The stage-specific pattern of seam cell division is coordinated by a genetic network that includes WNT asymmetry pathway components WRM-1, LIT-1, and POP-1, as well as heterochronic microRNAs (miRNAs) and their downstream targets. Mutations in pry-1, a negative regulator of WNT signaling that belongs to the Axin family, were shown to cause seam cell defects; however, the mechanism of PRY-1 action and its interactions with miRNAs remain unclear.
resultsWe found that pry-1 mutants in C. elegans exhibit seam cell, cuticle, and alae defects. To examine this further, a miRNA transcriptome analysis was carried out, which showed that let-7 (miR-48, miR-84, miR-241) and lin-4 (lin-4, miR-237) family members were upregulated in the absence of pry-1 function. Similar phenotypes and patterns of miRNA overexpression were also observed in C. briggsae pry-1 mutants, a species that is closely related to C. elegans. RNA interference-mediated silencing of wrm-1 and lit-1 in the C. elegans pry-1 mutants rescued the seam cell defect, whereas pop-1 silencing enhanced the phenotype, suggesting that all three proteins are likely important for PRY-1 function in seam cells. We also found that these miRNAs were overexpressed in pop-1 hypomorphic animals, suggesting that PRY-1 may be required for POP-1-mediated miRNA suppression. Analysis of the let-7 and lin-4-family heterochronic targets, lin-28 and hbl-1, showed that both genes were significantly downregulated in pry-1 mutants, and furthermore, lin-28 silencing reduced the number of seam cells in mutant animals.
conclusionsOur results show that PRY-1 plays a conserved role to maintain normal expression of heterochronic miRNAs in nematodes. Furthermore, we demonstrated that PRY-1 acts upstream of the WNT asymmetry pathway components WRM-1, LIT-1, and POP-1, and miRNA target genes in seam cell development.
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