PUBLICATION

Conserved and divergent functions of Nfix in skeletal muscle development during vertebrate evolution

Authors
Pistocchi, A., Gaudenzi, G., Foglia, E., Monteverde, S., Moreno-Fortuny, A., Pianca, A., Cossu, G., Cotelli, F., and Messina, G.
ID
ZDB-PUB-130403-11
Date
2013
Source
Development (Cambridge, England)   140(7): 1528-1536 (Journal)
Registered Authors
Cotelli, Franco
Keywords
Nfix, skeletal myogenesis, zebrafish, slow muscle fibers, sarcoplasmic reticulum
MeSH Terms
  • Animals
  • Animals, Genetically Modified
  • Conserved Sequence/physiology
  • Embryo, Mammalian
  • Embryo, Nonmammalian
  • Evolution, Molecular*
  • Genetic Speciation
  • Mice
  • Muscle Development/genetics
  • Muscle Development/physiology
  • Muscle, Skeletal/embryology*
  • Muscle, Skeletal/metabolism
  • NFI Transcription Factors/genetics
  • NFI Transcription Factors/physiology*
  • Phylogeny
  • Vertebrates/embryology
  • Vertebrates/genetics*
  • Vertebrates/physiology
  • Zebrafish/embryology
  • Zebrafish/genetics
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/physiology*
PubMed
23482488 Full text @ Development
Abstract

During mouse skeletal muscle development, the Nfix gene has a pivotal role in regulating fetal-specific transcription. Zebrafish and mice share related programs for muscle development, although zebrafish develops at a much faster rate. In fact, although mouse fetal muscle fibers form after 15 days of development, in fish secondary muscle fibers form by 48 hours post-fertilization in a process that until now has been poorly characterized mechanically. In this work, we studied the zebrafish ortholog Nfix (nfixa) and its role in the proper switch to the secondary myogenic wave. This allowed us to highlight evolutionarily conserved and divergent functions of Nfix. In fact, the knock down of nfixa in zebrafish blocks secondary myogenesis, as in mouse, but also alters primary slow muscle fiber formation. Moreover, whereas Nfix mutant mice are motile, nfixa knockdown zebrafish display impaired motility that probably depends upon disruption of the sarcoplasmic reticulum. We conclude that, during vertebrate evolution, the transcription factor Nfix lost some specific functions, probably as a consequence of the different environment in which teleosts and mammals develop.

Genes / Markers
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Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping