PUBLICATION

A novel TRIM family member, trim69, regulates zebrafish development through p53-mediated apoptosis

Authors
Han, R., Zhao, Q., Zong, S., Miao, S., Song, W., Wang, L.
ID
ZDB-PUB-160401-5
Date
2016
Source
Molecular reproduction and development   83(5): 442-54 (Journal)
Registered Authors
Song, Wei
Keywords
apoptosis, development, tp53, trim69, zebrafish
MeSH Terms
  • Animals
  • Animals, Genetically Modified/embryology
  • Animals, Genetically Modified/genetics
  • Apoptosis/physiology*
  • Embryo, Nonmammalian/embryology*
  • Embryonic Development/physiology*
  • Tripartite Motif Proteins/genetics
  • Tripartite Motif Proteins/metabolism*
  • Tumor Suppressor Protein p53/genetics
  • Tumor Suppressor Protein p53/metabolism*
  • Ubiquitin-Protein Ligases/genetics
  • Ubiquitin-Protein Ligases/metabolism
  • Zebrafish/embryology*
  • Zebrafish/genetics
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
PubMed
27031046 Full text @ Mol. Reprod. Dev.
Abstract
Trim69 contains the hallmark domains of a tripartite motif (TRIM) protein, including a Ring-finger domain, B-box domain, and coiled-coil domain. Trim69 is structurally and evolutionarily conserved in zebrafish, mouse, rat, human, and chimpanzee. The role of this protein is unclear, however, so we investigated its function in zebrafish development. Trim69 is extensively expressed in zebrafish adults and developing embryos - particularly in the testis, brain, ovary, and heart - and its expression decreases in a time- and stage-dependent manner. Loss of trim69 in zebrafish induces apoptosis and activates apoptosis-related processes; indeed, the tp53 pathway was up-regulated in response to the knockdown. Expression of human trim69 rescued the apoptotic phenotype, while overexpression of trim69 does not increase cellular apoptosis. Taken together, our results suggest that trim69 participates in tp53-mediated apoptosis during zebrafish development. This article is protected by copyright. All rights reserved.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping