PUBLICATION
MicroRNA-203a regulates fast muscle differentiation by targeting dmrt2a in zebrafish embryos
- Authors
- Lu, C., Wu, J., Xiong, S., Zhang, X., Zhang, J., Mei, J.
- ID
- ZDB-PUB-170510-9
- Date
- 2017
- Source
- Gene 625: 49-54 (Journal)
- Registered Authors
- Mei, Jie
- Keywords
- Fast muscle, Slow muscle, dmrt2a, miR-203
- MeSH Terms
-
- Animals
- DNA-Binding Proteins/genetics*
- DNA-Binding Proteins/metabolism
- Gene Expression Regulation, Developmental*
- MicroRNAs/genetics*
- Muscle, Skeletal/embryology
- Muscle, Skeletal/metabolism*
- Myosin Heavy Chains/genetics
- Myosin Heavy Chains/metabolism
- Transcription Factors/genetics*
- Transcription Factors/metabolism
- Zebrafish
- Zebrafish Proteins/genetics*
- Zebrafish Proteins/metabolism
- PubMed
- 28483596 Full text @ Gene
Citation
Lu, C., Wu, J., Xiong, S., Zhang, X., Zhang, J., Mei, J. (2017) MicroRNA-203a regulates fast muscle differentiation by targeting dmrt2a in zebrafish embryos. Gene. 625:49-54.
Abstract
Dmrt2b (doublesex and mab-3 related transcription factor 2b) has been revealed to be involved in zebrafish slow muscle development. However, the function of dmrt2a, a paralogue gene of dmrt2b, remains unclear during zebrafish muscle development. Here, we demonstrated that knockdown of dmrt2a resulted in severe developmental defects, and caused downregulation of fast muscle marker myhz-2 and upregulation of slow muscle marker myhz-5, respectively. It is known that microRNAs (miRNAs) control many biological events including muscle development. Dmrt2a was predicted to be a target gene of miR-203, which was further verified by luciferase reporter assay, since miR-203a was found to directly reduce the expression of dmrt2a by binding to the seed sequence of its 3'UTR. After miR-203a injection into zebrafish embryos, the expression of dmrt2a was significantly inhibited. Similar to the effect of dmrt2a knockdown, miR-203a overexpression led to downregulation of myhz-2 and upregulation of myhz-5. Our studies indicated that miR-203a directly regulated dmrt2a expression to control fast and slow muscle differentiation, while overexpression of miR-203a or knockdown of dmrt2a will impair fast muscle development and promote slow muscle development.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping