The knockdown of maternal glucocorticoid receptor mRNA alters embryo development in zebrafish

Dev Dyn. 2011 Apr;240(4):874-89. doi: 10.1002/dvdy.22586. Epub 2011 Feb 28.

Abstract

In zebrafish, ovulated oocytes contain both maternal cortisol and the mRNA for the glucocorticoid receptor (gr), which is spread as granular structures throughout the ooplasm. At 0.2 hpf, this transcript is relocated in the blastodisc area and partitioned among blastomeres. At 6-8 hpf, it is replaced by zygotic transcript. We used morpholinos to block translation of both maternal and zygotic gr transcripts, and a missplicing morpholino to block post-transcriptionally the zygotic transcript alone. Only knockdown of translation produced an increase of apoptosis and subsequent craniofacial and caudal deformities with severe malformations of neural, vascular, and visceral organs in embryos and 5-dpf larvae. Such defects were rescued with trout gr2 mRNA. Microarray analysis revealed that 114 and 37 highly expressed transcripts were up- and down-regulated, respectively, by maternal Gr protein deficiency in 5-hpf embryos. These results indicate that the maternal gr transcript and protein participate in the maternal programming of zebrafish development.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Animals, Genetically Modified
  • Apoptosis / genetics
  • Apoptosis / physiology
  • Base Sequence
  • Embryo, Nonmammalian
  • Embryonic Development / genetics*
  • Female
  • Gene Expression Regulation, Developmental
  • Gene Knockdown Techniques
  • Larva / genetics
  • Larva / growth & development
  • Larva / metabolism
  • Molecular Sequence Data
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • RNA, Messenger, Stored / genetics*
  • RNA, Messenger, Stored / metabolism
  • Receptors, Glucocorticoid / genetics*
  • Receptors, Glucocorticoid / metabolism
  • Zebrafish / embryology*
  • Zebrafish / genetics*
  • Zebrafish / metabolism

Substances

  • RNA, Messenger
  • RNA, Messenger, Stored
  • Receptors, Glucocorticoid