PUBLICATION

Knock-Down of Histidyl-tRNA Synthetase Causes Cell Cycle Arrest and Apoptosis of Neuronal Progenitor Cells in vivo

Authors
Waldron, A., Wilcox, C., Francklyn, C., Ebert, A.
ID
ZDB-PUB-190528-33
Date
2019
Source
Frontiers in cell and developmental biology   7: 67 (Journal)
Registered Authors
Keywords
CCND1, Cyclin D1, HARS, aminoacyl-tRNA synthetase, apoptosis, histidyl-tRNA synthetase, proliferation, retina
MeSH Terms
none
PubMed
31134197 Full text @ Front Cell Dev Biol
Abstract
Histidyl-tRNA Synthetase (HARS) is a member of the aminoacyl-tRNA synthetase family, which attach amino acids to their associated tRNA molecules. This reaction is a crucial step in protein synthesis that must be carried out in every cell of an organism. However, a number of tissue-specific, human genetic disorders have been associated with mutations in the genes for aminoacyl-tRNA synthetases, including HARS. These associations indicate that, while we know a great deal about the molecular and biochemical properties of this enzyme, we still do not fully understand how these proteins function in the context of an entire organism. To this end, we set out to knock-down HARS expression in the zebrafish and characterize the developmental consequences. Through our work we show that some tissues, particularly the nervous system, are more sensitive to HARS loss than others and we reveal a link between HARS and the proliferation and survival of neuronal progenitors during development.
Genes / Markers
Figures
Figure Gallery
Expression
Phenotype
Mutation and Transgenics
Human Disease / Model Data
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping
Errata and Notes