MiR-430 is considered an important regulator during embryonic development, but genetic loss-of-function study is still lacking. Here we demonstrated that genetic deletion of the miR-430 cluster resulted in developmental defects in cell movement, germ layer specification, axis patterning and organ progenitor formation in zebrafish. Transcriptome analysis indicated that the maternally provided transcripts were not properly degraded whereas the zygotic genome expressed genes were not fully activated in the miR-430 mutants. We further found that a reciprocal regulatory loop exists between miR-430 and maternally provided transcripts: the maternally provided transcripts (Nanog, Dicer1, Dgcr8, and AGOs) are required for miR-430 biogenesis and function, whereas miR-430 is required for the clearance of these maternally provided transcripts. These data provide the first genetic evidence that miR-430 is required for maternal-zygotic transition and subsequent establishment of embryonic body plan.

MiR-430被认为是胚胎发育过程中的重要调控因子，但仍缺乏基因功能丧失研究。在这里，我们证明了miR-430团簇导致斑马鱼细胞运动，胚层规格，轴模式和器官祖细胞形成的发育缺陷。转录组分析表明，母本提供的转录本未正确降解，而合子基因组表达的基因并未完全激活。miR-430突变体。我们进一步发现，在两个miR-430 以及由母亲提供的成绩单：由母亲提供的成绩单（纳诺克， Dicer1， Dgcr8和 非政府组织是的 miR-430 生物发生和功能，而 miR-430需要清除这些由母亲提供的成绩单。这些数据提供了第一个遗传证据，miR-430 是母体-合子过渡和随后建立胚胎身体计划所必需的。