Abstract
Skeletal muscles are readily characterized by their location within the body and by the number and composition of their constituent muscle fibers. Here, we characterize a mutation that causes a severe reduction in the number of fibers comprising the tergal depressor of the trochanter muscle (TDT, or jump muscle), which functions in the escape response of the Drosophila adult. The wild-type TDT comprises over 20 large muscle fibers and four small fibers. In crossveinless (cv) mutants, the number of large fibers is reduced by 50%, and the number of small fibers is also occasionally reduced. This reduction in fiber number arises from a reduction in the number of founder cells contributing to the TDT at the early pupal stage. Given the role of cv in TGFbeta signaling, we determined whether this pathway directly impacts TDT development. Indeed, gain- and loss-of-function manipulations in the TGFbeta pathway resulted in dramatic increases and decreases, respectively, in TDT fiber number. By identifying the origins of the TDT muscle, from founder cells specified in the mesothoracic leg imaginal disc, we also demonstrate that the TGFbeta pathway directly impacts the specification of founder cells for the jump muscle. Our studies define a new role for the TGFbeta pathway in the control of specific skeletal muscle characteristics.