ArticleDevelopmental dynamics : an official publication of the American Association of Anatomists2017
Putative binding sites for mir-125 family miRNAs in the mouse Lfng 3'UTR affect transcript expression in the segmentation clock, but mir-125a-5p is dispensable for normal somitogenesis.
Article in Developmental dynamics : an official publication of the American Association of Anatomists, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 4 citations in OpenAlex.
- Keeping development on time: Insights into post-transcriptional mechanisms driving oscillatory gene expression during vertebrate segmentation.Wiley interdisciplinary reviews. RNA · 2023Review
- Species-specific roles of the Notch ligands, receptors, and targets orchestrating the signaling landscape of the segmentation clock.Frontiers in cell and developmental biology · 2023Review
- The vertebrate Embryo Clock: Common players dancing to a different beat.Frontiers in cell and developmental biology · 2022Review
- Sweet Control: MicroRNA Regulation of the Glycome.Biochemistry · 2020Review
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4 authors at 2 institutions in 1 country.
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Abstract
backgroundIn vertebrate embryos, a "segmentation clock" times somitogenesis. Clock-linked genes, including Lunatic fringe (Lfng), exhibit cyclic expression in the presomitic mesoderm (PSM), with a period matching the rate of somite formation. The clock period varies widely across species, but the mechanisms that underlie this variability are not clear. The half-lives of clock components are proposed to influence the rate of clock oscillations, and are tightly regulated in the PSM. Interactions between Lfng and mir-125a-5p in the embryonic chicken PSM promote Lfng transcript instability, but the conservation of this mechanism in other vertebrates has not been tested. Here, we examine whether this interaction affects clock activity in a mammalian species.
resultsMutation of mir-125 binding sites in the Lfng 3'UTR leads to persistent, nonoscillatory reporter transcript expression in the caudal-most mouse PSM, although dynamic transcript expression recovers in the central PSM. Despite this, expression of endogenous mir-125a-5p is dispensable for mouse somitogenesis.
conclusionsThese results suggest that mir-125a sites in the Lfng 3' untranslated region influence transcript turnover in both mouse and chicken embryos, and support the existence of position-dependent regulatory mechanisms in the PSM. They further suggest the existence of compensatory mechanisms that can rescue the loss of mir-125a-5p in mice. Developmental Dynamics 246:740-748, 2017. © 2017 Wiley Periodicals, Inc.
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