High impact information on myf5

• In normal development, zygotic expression of SL1 (MEF2D) precedes that of SL2 (MEF2A) by several hours, but neither gene is expressed prior to the accumulation of MyoD and Myf5 transcripts in the somitic mesoderm [1].
• Ectopic expression of the myogenic factors in explants of presumptive ectoderm induces expression of both SL1 and SL2, whereas in reciprocal experiments, neither RSRF protein activates the endogenous myoD or Myf5 genes [1].
• (1998 [this issue of Neuron]) identify ngns as vertebrate neuronal determination genes, analogous to myoD and myf5 in myogenesis [2].
• To study the in vivo effects of overexpressing Xenopus MyoD and Myf5, synthetic RNAs were microinjected into single blastomeres of 2- to 32-cell stage Xenopus embryos [3].
• A T-box binding site has been identified in the Xenopus Myf5 promoter, and in other species, T-box genes have been implicated in myogenic fate [4].

Biological context of myf5

• To this end we have cloned and sequenced Xenopus tropicalis homologues of Myf5 and MyoD and found a high degree of conservation in the nucleotide and amino acid sequences of both genes [5].
• CMHC gene expression is induced in ectodermal cells of the animal cap in blastula-stage embryos injected with synthetic MyoD or Myf5 RNA, suggesting that the CMHC gene contains regulatory elements that are responsive to the activity of those skeletal-muscle-specific transcription factors [6].

Anatomical context of myf5

• Chordin diverted somatic muscle cells to more anterior positions within the somite file in chordin-induced secondary trunks and induced the expression of the anterior myogenic gene myf5 [7].

References