The zebrafish gene mission impossible/dhx16 has a maternal role in downstream events of the zygotic endoderm specification pathway and morphogenesis.

摘要

Embryonic development begins with the fertilization of an oocyte by a sperm. The ensuing developmental events, including fusion of the pronuclei, initiation of mitosis, and cellularization, are driven by maternally and paternally provided gene products. In the vertebrate zebrafish Danio rerio, perduring maternal factors continue to function in developmental programs for cell fate specification and morphogenesis even after zygotic gene expression has initiated. Analyses of mutations in these maternal factors provide a framework for understanding the molecular controls of early vertebrate development.;The zebrafish mutation mission impossible ( mis) is a recessive maternal-effect mutation that affects early embryogenesis after the initiation of zygotic gene transcription. Maternal mis embryos show extensive morphogenesis defects which are manifested in a severe delay of epiboly progression and reduction of gastrulation. All cell layers of the embryo behave aberrantly in maternal mis embryos, and deep layer cells are cell autonomously affected in their motility. Furthermore, maternal mis embryos show a severe deficiency in the induction of the endodermal germ layer, but the ectodermal and mesodermal germ layers appear to be induced normally. Specifically, the mis mutation eliminates the response to overexpression of the Nodal-related genes squint and cyclops as assayed by the endodermal target gene sox-17. Maternal mis embryos can, however, induce the endodermal gene sox-32/casanova and the mesodermal gene no tail in response to Nodal overexpression. Thus, mis acts very specifically in the Nodal pathway for endoderm specification downstream of sox-32/casanova for the induction of sox-17. Molecular cloning of mis shows that it encodes the gene DEAH-box16 a conserved RNA helicase, and injection of mRNA encoding dhx16 rescues the mis mutant phenotype. I propose that DEAH-box16/mis plays a role in the post-transcriptional regulation of a subset of transcripts involved in the specification of endoderm and embryonic morphogenesis.