PUBLICATION

Coordination of development and metabolism in the pre-midblastula transition zebrafish embryo

Authors
Mendelsohn, B.A., and Gitlin, J.D.
ID
ZDB-PUB-080610-12
Date
2008
Source
Developmental Dynamics : an official publication of the American Association of Anatomists   237(7): 1789-1798 (Journal)
Registered Authors
Gitlin, Jonathan D.
Keywords
zebrafish, anoxia, mitochondria, epiboly, midblastula transition, AMPK
MeSH Terms
  • AMP-Activated Protein Kinases/metabolism
  • Animals
  • Blastula/cytology
  • Blastula/metabolism*
  • Cell Cycle/drug effects
  • Embryo, Nonmammalian/cytology
  • Embryo, Nonmammalian/metabolism*
  • Immunoblotting
  • Mitochondria/drug effects
  • Mitochondria/metabolism
  • Oxidative Phosphorylation/drug effects
  • Potassium Cyanide/pharmacology
  • Transcription, Genetic/genetics
  • Zebrafish/embryology
  • Zebrafish/metabolism*
  • Zebrafish Proteins/metabolism
PubMed
18521947 Full text @ Dev. Dyn.
Abstract
To define the mechanisms that coordinate early embryonic development and metabolism, we have examined the response of zebrafish embryos to anoxia before the midblastula transition. Our findings reveal that anoxic pre-midblastula transition embryos slow the cell cycle, arrest before the midblastula transition and can recover normally if restored to a normoxic environment. Analyses of respiratory rates reveal that pre-midblastula transition embryos are less reliant on oxidative phosphorylation than older embryos. Interestingly, arrest in anoxia occurs despite inhibition of zygotic transcription, revealing a central role for maternal factors in the response to energy limitation. Consistent with this concept, we demonstrate that the posttranslational energy-sensing AMP-activated protein kinase pathway is activated in anoxia in pre-midblastula transition embryos. Taken together, these findings demonstrate a maternal program capable of coordinating developmental rate and metabolism in the absence of transcription-based pathways or cell cycle checkpoints.
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