In wild-type embryos of Drosophila melanogaster, the formation of diff
erentiated larval muscles is preceded by the segregation of small numb
ers of progenitor or founder cells in the embryonic mesoderm. The foun
der cells, characterised by the expression of genes encoding putative
transcription factors such as S59 or vestigial, fuse with neighbouring
myoblasts to form syncytial precursors of individual muscles. Founder
cell segregation is deranged in embryos mutant for any of the neuroge
nic genes: enlarged clusters of cells expressing S59 or vestigial are
detected at the sites where small numbers of founder cells segregate i
n the wild type. In addition, muscle differentiation is deranged in su
ch embryos in a way that appears to be closely linked to the extent of
epidermal disruption caused by the neurogenic phenotype: myoblast fus
ion is limited to regions of the mesoderm beneath the residual epiderm
is left by the hyperplasia of the nervous system, and late expression
of S59 and vestigial is lost from mesoderm not lying within the margin
s of the residual epidermis. Thus neurogenic gene functions appear to
be required both for the normal segregation of founder cells and for m
uscle differentiation. It is not clear, whether either of these requir
ements reflects an essential function for any or all of the neurogenic
genes within the mesoderm itself.