PUBLICATION
Gli2 mediation of Hedgehog signals in slow muscle induction in zebrafish
- Authors
- Du, S.J. and Dienhart, M.
- ID
- ZDB-PUB-010416-5
- Date
- 2001
- Source
- Differentiation; research in biological diversity 67(3): 84-91 (Journal)
- Registered Authors
- Du, Shao Jun (Jim)
- Keywords
- zebrafish; slow muscle; fast muscle; hedgehog; Glis
- MeSH Terms
-
- Animals
- Embryo, Nonmammalian/metabolism*
- Embryonic Induction/genetics
- Embryonic Induction/physiology*
- Hedgehog Proteins
- Immunohistochemistry
- In Situ Hybridization
- In Vitro Techniques
- Microinjections
- Muscle Fibers, Fast-Twitch/cytology
- Muscle Fibers, Fast-Twitch/physiology
- Muscle Fibers, Slow-Twitch/cytology
- Muscle Fibers, Slow-Twitch/physiology*
- Muscle, Skeletal/cytology
- Muscle, Skeletal/embryology
- Mutation
- Proteins/genetics
- Proteins/metabolism*
- RNA, Messenger/genetics
- RNA, Messenger/metabolism*
- Signal Transduction
- Trans-Activators*
- Transcription Factors/metabolism*
- Zebrafish/embryology*
- Zebrafish/metabolism
- Zebrafish Proteins*
- Zinc Fingers/genetics
- Zinc Fingers/physiology*
- PubMed
- 11428131 Full text @ Differentiation
Citation
Du, S.J. and Dienhart, M. (2001) Gli2 mediation of Hedgehog signals in slow muscle induction in zebrafish. Differentiation; research in biological diversity. 67(3):84-91.
Abstract
Zebrafish skeletal muscles are composed of two major types of muscle fibers, broadly classified as fast or slow fibers. Recent studies have demonstrated that members of the Hedgehog (Hh) family induce the formation of slow muscle fibers. Hedgehog signals are secreted proteins that function through the transcription factor Glis. We report here the characterization of a zebrafish Gli2 expression in slow and fast muscle cells and the study of the roles of Hedgehogs and Gli2 in zebrafish muscle development using two mutant strains; sonic-you (syu) and you-too (yot), respective for sonic hedgehog (shh) and Gli2 mutation. We have demonstrated that Shh and Gli2 mutation causes similar defects in slow muscle formation. There is, however, a difference in the degree of defect between these two mutants. In yot mutant embryos, development of slow muscles was completely blocked, whereas in syu mutant embryos, a small number of slow muscle cells could still form, suggesting that other Hhs were also involved in slow muscle induction. Induction of slow muscles by other Hhs appeared to require Gli2, because ectopic expression of Echidna hedgehog (Ehh) and Tiggy-winkle hedgehog (Twhh) failed to induce slow muscles in yot mutant embryos. Together, these data suggest that further Hhs, other than Shh, are also involved in the induction and differentiation of slow muscle cells and that Gli2 is required by Shh, Twhh, and Ehh, thus playing a key role in the induction and differentiation of slow muscle cells.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping