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Maternal miR-202-5p is required for zebrafish primordial germ cell migration by protecting small GTPase Cdc42.
Journal of Molecular Cell Biology ( IF 5.5 ) Pub Date : 2019-11-19 , DOI: 10.1093/jmcb/mjz103
Yilin Jin 1, 2, 3 , Wei Liu 1, 2, 3 , Yangxi Xiang 1, 2, 3 , Wanwan Zhang 1, 2, 3 , Hong Zhang 1, 2, 3 , Kuntong Jia 1, 2, 3 , Meisheng Yi 1, 2, 3
Affiliation  

In many lower animals, germ cell formation, migration and maintenance depend on maternally provided determinants in germ plasm. In zebrafish, these processes have been extensively studied in terms of RNA binding proteins and other coding genes. The role of small non-coding RNAs in the regulation of primordial germ cell (PGC) development remains largely unknown and poorly investigated, even though growing interests for the importance of miRNAs involved in a wide variety of biological processes. Here, we reported the role and mechanism of the germ plasm-specific miRNA miR-202-5p in PGC migration; (i) both maternal loss and knockdown of miR-202-5p impaired PGC migration indicated by the mislocalization and reduced number of PGCs, (ii) cdc42se1 was a direct target gene of miR-202-5p, and overexpression of Cdc42se1 in PGCs caused PGC migration defects similar to those observed in loss of miR-202-5p mutants; (iii) Cdc42se1 not only interacted with Cdc42, but also inhibited cdc42 transcription, and overexpression of Cdc42 could rescue PGC migration defects in Cdc42se1 overexpressed embryos. Thus, miR-202-5p regulates PGC migration by directly targeting and repressing Cdc42se1 to protect the expression of Cdc42, which interacts with Actin to direct PGC migration.

中文翻译:

通过保护小 GTPase Cdc42,母体 miR-202-5p 是斑马鱼原始生殖细胞迁移所必需的。

在许多低等动物中,生殖细胞的形成、迁移和维持取决于生殖质中母体提供的决定因素。在斑马鱼中,这些过程在 RNA 结合蛋白和其他编码基因方面得到了广泛研究。小非编码 RNA 在调节原始生殖细胞 (PGC) 发育中的作用仍然很大程度上未知且研究不足,尽管人们对 miRNA 在各种生物过程中的重要性越来越感兴趣。在这里,我们报道了种质特异性 miRNA miR-202-5p 在 PGC 迁移中的作用和机制;(i) 母体丢失和 miR-202-5p 的敲低均损害了 PGC 迁移,由错误定位和 PGC 数量减少表明,(ii) cdc42se1 是 miR-202-5p 的直接靶基因,Cdc42se1 在 PGC 中的过表达导致 PGC 迁移缺陷,类似于在 miR-202-5p 突变体缺失中观察到的缺陷;(iii) Cdc42se1 不仅与 Cdc42 相互作用,还抑制了 cdc42 的转录,Cdc42 的过表达可以挽救 Cdc42se1 过表达胚胎中的 PGC 迁移缺陷。因此,miR-202-5p 通过直接靶向和抑制 Cdc42se1 来调节 PGC 迁移,以保护 Cdc42 的表达,Cdc42 与肌动蛋白相互作用以指导 PGC 迁移。
更新日期:2019-11-19
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