PUBLICATION

Suppression of myostatin with vector-based RNA interference causes a double-muscle effect in transgenic zebrafish

Authors
Lee, C.Y., Hu, S.Y., Gong, H.Y., Chen, M.H., Lu, J.K., and Wu, J.L.
ID
ZDB-PUB-090731-9
Date
2009
Source
Biochemical and Biophysical Research Communications   387(4): 766-771 (Journal)
Registered Authors
Gong, Hong-Yi, Lee, Chiou-Yueh, Wu, Jen-Leih
Keywords
Myostatin, Zebrafish, RNA interference
MeSH Terms
  • Animals
  • Animals, Genetically Modified/embryology*
  • Animals, Genetically Modified/genetics
  • Gene Expression Regulation, Developmental
  • Gene Knockdown Techniques
  • Models, Animal
  • Muscle Development*
  • Muscles/embryology*
  • Myostatin/genetics*
  • RNA Interference
  • RNA, Small Interfering/genetics
  • Zebrafish/embryology*
  • Zebrafish/genetics
  • Zebrafish Proteins/genetics*
PubMed
19635460 Full text @ Biochem. Biophys. Res. Commun.
Abstract
Myostatin belongs to the transforming growth factor (TGF)-beta superfamily and is a potent negative regulator of skeletal muscle development and growth. We utilized microinjection of an antisense RNA-expressing vector to establish a hereditarily stable myostatin gene knockdown zebrafish strain with a double-muscle phenotype. Real-time PCR and immunostaining revealed that the myostatin messenger (m)RNA and protein levels in homozygous transgenic zebrafish were 33% and 26% those of the non-transgenic controls, respectively. Also, the mRNA levels of myogenic regulatory factor markers such as MyoD, myogenin, Mrf4, and Myf5 were dramatically elevated in myostatin-suppressed transgenic fish compared to the non-transgenic controls. Although there was no significant difference in body length, homozygous transgenic zebrafish were 45% heavier than non-transgenic controls. Histochemical analysis showed that the cross-sectional area of the muscle fiber of homozygous transgenic fish was twice as large as that of non-transgenic controls. This is the first model zebrafish with a hereditarily stable myostatin-suppressed genotype and a double-muscle phenotype.
Genes / Markers
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping