Fig. 1

Myod protein level correlates with slow myogenesis in Hh signalling mutants. In situ mRNA hybridization for myf5, myod, myog and hsp90a and immunodetection of Myod and Myosin Heavy Chain (MyHC) in dorsal flatmounts of 5 ss stage control, cyclopamine-treated (cyA), smo^b641 and shha^tbx392 mutant embryos. Mutants were identified by significant reduction in one or both markers in ~ 25% of lay (shha^tbx392: 9/41; smo^b641 14/50). Anterior to top. Bar: 100 μm. (A). Absence of MyHC in smo^b641 but only reduction in shha^tbx392 mutants, despite indistinguishable loss of myod and myf5 mRNAs in adaxial cells in anterior pre-somitic mesoderm (arrows). Note that myf5 and myod expression in tailbud (asterisk) and presumptive fast muscle precursors (black arrowheads) is little affected by Hh manipulation. Shha^tbx392 differs from smo^b641 only in expression of myod in differentiating adaxial muscle in somites (white arrowheads). (B). Myog mRNA is present in adaxial cells of shha^tbx392 but not smo^b641 mutants. (C). Myod protein is absent in adaxial cells of cyA and smo^b641 embryos but weakly present in shha^tbx392 mutant. Control embryos were either shha^tbx392 siblings or untreated wild type.