Oligoasthenoteratozoospermia and infertility in mice deficient for miR-34b/c and miR-449 loci.

Oligoasthenoteratozoospermia and infertility in mice deficient for miR-34b/c and miR-449 loci.

Blog Article

Male fertility requires the continuous production of high quality motile spermatozoa in abundance.Alterations in all three metrics cause oligoasthenoteratozoospermia, the leading cause of human sub/infertility.Post-mitotic spermatogenesis inclusive of several meiotic stages and spermiogenesis (terminal spermatozoa differentiation) are transcriptionally inert, indicating the potential importance for the post-transcriptional microRNA (miRNA) gene-silencing pathway therein.We found the expression of miRNA 7-Piece Power Reclining Sectional generating enzyme Dicer within spermatogenesis peaks in meiosis with critical functions in spermatogenesis.In an expression screen we identified two miRNA loci of the miR-34 family (miR-34b/c and miR-449) that are specifically and highly expressed in post-mitotic male germ cells.

A reduction in several miRNAs inclusive of miR-34b/c in spermatozoa has been causally associated with reduced fertility in humans.We found that deletion of both miR34b/c and miR-449 loci resulted in oligoasthenoteratozoospermia in mice.MiR-34bc/449-deficiency impairs both meiosis and the final stages of spermatozoa maturation.Analysis of miR-34bc-/-;449-/- pachytene spermatocytes revealed a small cohort of genes deregulated that were highly enriched for miR-34 family target Bread genes.Our results identify the miR-34 family as the first functionally important miRNAs for spermatogenesis whose deregulation is causal to oligoasthenoteratozoospermia and infertility.