Abstract
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.
Highlights
MicroRNAs are ∼22-nucleotide non-coding RNAs that repress mRNA expression post-transcriptionally (Bartel, 2009)
We have characterized the phenotypes of miR-430 homozygous mutants
Whole mount in situ hybridization analysis indicated that the primary miR-430 transcript was abundantly expressed in the WT (4 hpf) but not in the miR-430 mutants (Figure 1B)
Summary
MicroRNAs (miRNAs) are ∼22-nucleotide (nt) non-coding RNAs that repress mRNA expression post-transcriptionally (Bartel, 2009). Transcribed by RNA polymerase II, the primary miRNA transcripts are processed by Dgcr and RNase III enzyme Drosha into 70-nt precursors which are further processed into 21–23-nt mature microRNAs by Dicer (Kim et al, 2009). One strand of the mature microRNAs is loaded into argonaute (AGO) protein to recognize target mRNAs by pairing with miRNA binding sites in the 3 untranslated region (UTR) (Kim et al, 2009). One miRNA can modulate hundreds of mRNA targets and more than 60% of human protein-coding genes are considered targets for miRNAs (Friedman et al, 2009)
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