HLH54F^Δ598 mutants exhibit a loss of caudal visceral mesoderm markers at all stages and the failure of cellular rearrangements and movements in the caudal visceral mesoderm suggest that HLH54F is required for specification of the caudal visceral mesoderm and longitudinal visceral muscles. As a consequence of the absence of these muscles, midgut constrictions are not formed efficiently and a small fraction of HLH54F^Δ598 homozygous and HLH54F^Δ598/HLH54F^S1750 transheterozygous mutant embryos lack midgut constrictions altogether. Midguts isolated from mutant adults tend to be more curled into a spiral shape and smaller in diameter than their straighter wild-type counterparts. The adult mutant gut tube exhibits small bulges and frequently shows melanotic masses, suggesting a tendency to rupture in vivo. In addition to the absence of support by longitudinal muscle fibers, this apparent fragility of adult midguts may be explained by the presence of highly disordered circular muscle fibers that show frequent interruptions.

HLH54F^Δ598 mutants exhibit an increase in TUNEL-positive cells in stage 12 embryos, indicating an increase in apoptosis.

HLH54F^Δ598 has increased cell death phenotype, suppressible by Scer\GAL4^byn-Gal4/BacA\p35^UAS.cHa

HLH54F^Δ598 has longitudinal trunk visceral muscle primordium phenotype, suppressible by Scer\GAL4^byn-Gal4/BacA\p35^UAS.cHa