mef2 encodes the only apparent Drosophila homolog of the vertebrate my
ocyte-specific enhancer factor 2 (MEF2). We show herein that the Droso
phila MEF2 protein is expressed throughout the mesoderm following gast
rulation. Later in embryogenesis, its expression is maintained in prec
ursors and differentiated cells of the somatic and visceral musculatur
e, as well as the heart. We have characterized genetic deficiencies an
d EMS-induced point mutations that result in complete loss of MEF2 pro
tein in homozygous mutant embryos. These embryos exhibit a dramatic ab
sence of myosin heavy chain (MHC)-expressing myoblasts and lack differ
entiated muscle fibers. Examination of earlier events of muscle develo
pment indicates that the specification and early differentiation of so
matic muscle precursors are not affected because even-skipped-, nautil
us-, and beta 3-tubulin-expressing myoblasts are present. However, the
se partially differentiated cells are unable to undergo further differ
entiation to form muscle fibers in the absence of mef2. The later aspe
cts of differentiation of the visceral mesoderm and the heart are also
disrupted in mef2 mutant embryos, although the specification and earl
y development of these tissues appear unaffected. Midgut morphogenesis
is disrupted in the mutant embryos, presumably as a consequence of ab
normal development of the visceral mesoderm. In the heart, the cardial
cells do not express MHC. These results indicate that MEF2 is require
d for later aspects of differentiation of the three major types of mus
culature, which include body wall muscles, gut musculature, and the he
art, in the Drosophila embryo.