PUBLICATION
Small ubiquitin-related modifier paralogs are indispensable but functionally redundant during early development of zebrafish
- Authors
- Yuan, H., Zhou, J., Deng, M., Liu, X., Bras, M.L., The, H.D., Chen, S.J., Chen, Z., Liu, T.X., and Zhu, J.
- ID
- ZDB-PUB-090828-22
- Date
- 2010
- Source
- Cell Research 20(2): 185-196 (Journal)
- Registered Authors
- Deng, Min
- Keywords
- SUMO paralogs, zebrafish, p53
- MeSH Terms
-
- Oligonucleotide Array Sequence Analysis
- Animals
- Gene Expression Profiling
- Humans
- Molecular Sequence Data
- Zebrafish/embryology*
- Zebrafish/genetics*
- Zebrafish/metabolism
- Genetic Complementation Test
- Embryo, Nonmammalian
- Amino Acid Sequence
- Sequence Homology
- Small Ubiquitin-Related Modifier Proteins/genetics
- Small Ubiquitin-Related Modifier Proteins/metabolism
- Small Ubiquitin-Related Modifier Proteins/physiology*
- Cells, Cultured
- Gene Expression Regulation, Developmental
- Protein Processing, Post-Translational/genetics
- Animals, Genetically Modified
- Embryonic Development/genetics*
- PubMed
- 19704416 Full text @ Cell Res.
Citation
Yuan, H., Zhou, J., Deng, M., Liu, X., Bras, M.L., The, H.D., Chen, S.J., Chen, Z., Liu, T.X., and Zhu, J. (2010) Small ubiquitin-related modifier paralogs are indispensable but functionally redundant during early development of zebrafish. Cell Research. 20(2):185-196.
Abstract
The Small ubiquitin-related modifier (SUMO) conjugation to a variety of proteins regulates diverse cellular processes, including transcription, cell cycle regulation and maintenance of genome integrity. To investigate in vivo biological function of SUMO paralogs, we inactivated them in the early development of zebrafish. While zebrafish embryos deficient for all three SUMO paralogs, as Ubc9-deficient ones, displayed severe defects, loss of individual SUMO paralog was compatible with a normal development. SUMO-deficient embryos can be rescued by a single human or zebrafish SUMO. While key structural basic lysine residues and N-terminal unstructured stretch of SUMO are critical for in vivo rescue, the consensus K11 sumoylation site of SUMO2 is dispensable, implying that chain formation on this potential site is unessential for normal development. Inactivation of all three SUMOs triggered p53-dependent apoptosis and further inactivation of p53 restored normal zebrafish development. Interestingly, we also demonstrate that the dominant negative truncated form of p53, Delta113p53, significantly blunts SUMO depletion-induced p53 activity in vivo. Taken together, our results suggest that SUMO paralogs are indispensable, but redundant, in the early development of zebrafish.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping