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.
Citation
Mendelsohn, B.A., and Gitlin, J.D. (2008) Coordination of development and metabolism in the pre-midblastula transition zebrafish embryo. Developmental Dynamics : an official publication of the American Association of Anatomists. 237(7):1789-1798.
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.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping