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miRNA regulation of Sdf1 chemokine signaling provides genetic robustness to germ cell migration.miRNA 对 Sdf1 趋化因子信号的调节为生殖细胞迁移提供了遗传稳定性。
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Embryonic stem cell-specific microRNAs promote induced pluripotency.胚胎干细胞特异性微小RNA促进诱导多能性。
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Embryonic stem cell-specific microRNAs regulate the G1-S transition and promote rapid proliferation.胚胎干细胞特异性微小RNA调控G1-S期转换并促进快速增殖。
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miR-290-295 缺失的小鼠表现为部分显性胚胎致死和生殖细胞缺陷。

Mir-290-295 deficiency in mice results in partially penetrant embryonic lethality and germ cell defects.

机构信息

Whitehead Institute for Biomedical Research, Cambridge, MA 02139, USA.

出版信息

Proc Natl Acad Sci U S A. 2011 Aug 23;108(34):14163-8. doi: 10.1073/pnas.1111241108. Epub 2011 Aug 15.

DOI:10.1073/pnas.1111241108
PMID:21844366
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3161528/
Abstract

Mir-290 through mir-295 (mir-290-295) is a mammalian-specific microRNA (miRNA) cluster that, in mice, is expressed specifically in early embryos and embryonic germ cells. Here, we show that mir-290-295 plays important roles in embryonic development as indicated by the partially penetrant lethality of mutant embryos. In addition, we show that in surviving mir-290-295-deficient embryos, female but not male fertility is compromised. This impairment in fertility arises from a defect in migrating primordial germ cells and occurs equally in male and female mutant animals. Male mir-290-295(-/-) mice, due to the extended proliferative lifespan of their germ cells, are able to recover from this initial germ cell loss and are fertile. Female mir-290-295(-/-) mice are unable to recover and are sterile, due to premature ovarian failure.

摘要

miR-290 到 miR-295（miR-290-295）是哺乳动物特异性 microRNA（miRNA）簇，在小鼠中，其特异性在早期胚胎和胚胎生殖细胞中表达。在这里，我们表明，miR-290-295 在胚胎发育中起着重要作用，突变胚胎的部分穿透致死性表明了这一点。此外，我们表明，在存活的 miR-290-295 缺陷胚胎中，雌性但不是雄性的生育能力受到损害。这种生育能力的损害源于迁移原始生殖细胞的缺陷，并且在雄性和雌性突变动物中同样发生。由于其生殖细胞的延长增殖寿命，雄性 miR-290-295（-/-）小鼠能够从这种初始生殖细胞损失中恢复，并且具有生育能力。由于卵巢早衰，雌性 miR-290-295（-/-）小鼠无法恢复，并且不育。