Abstract
bendless- (ben-) is an X chromosome mutation in Drosophila melanogaster, known to alter patterns of connections in the CNS and thus modify behavior (Thomas and Wyman, 1984). We report that in addition to its CNS effects, ben- has pleiotropic phenotypes affecting thoracic muscle patterning, pupal mortality, and post-eclosional mobility. The tergal depressor of the trochanter (TDT) normally attaches ventrally to an apodeme on the trochanter and dorsally to the lateral scutum just posterior to the intrascutal suture. In ben- individuals, TDT may attach anywhere within the boundaries of the attachment areas for TDT and dorsoventral muscles I (DVM I) and II (DVM II). Furthermore, TDT may completely lack a dorsal attachment, although it still maintains a ventral attachment. DVMs may also attach abnormally to dorsal sites normally occupied by an adjacent DVM, or may be entirely eliminated. DVM loss occurs independently of the position or presence of TDT dorsal attachment. The cytology of ben- TDT is altered. Muscles may have fibers that are swollen and stain abnormally. Other fibers may have large, axially aligned holes. ben- flies have an increased likelihood of failing to eclose and, upon eclosion, show impaired mobility. We describe several possible mechanisms for the ben- developmental defects and discuss this mutation in light of its evolutionary significance.
