Mutant embryos have proventriculus and hindgut defects.
Mutant embryos at stage 16 have hindguts about half the size of wild-type. These hindguts have larger lumens and two or three more cells in their circumference than those of wild-type. Hindguts are club shaped and smaller in both length and diameter. Hindgut epithelial cells are taller and narrower than seen in wild-type. The "boundary cells" that normally run the length of the large intestine are duplicated. Cell proliferation and apoptosis appear normal in mutant hindguts. Hindguts contain slightly fewer cells than wild-type. The visceral mesoderm is also normal in these mutants.
drm1 is not embryonic lethal. Homozygous embryos show defects in hindgut elongation and folding of the proventriculus, but do not show any defects in other epithelial structures. The hindgut is shorter and wider than normal.
Isolation: drm1 was identified in the 'l(2)k11011' line, which contains two P{lacW} insertions; P{lacW}k11011a and P{lacW}ak11011b. Mapping indicates that drm1 is not caused by either P{lacW} insertion. The chromosome carries an embryonic lethal mutation that is separable from drm1.
drm alleles form an allelic series: drm5 < drm2 < drm4 < drm1 < drm6 = drm3 < Df(2L)drm-P1 = Df(2L)drm-P2.
drm alleles form an allelic series: drm5 < drm2 < drm4 < drm1 < drm3 = drm6 < Df(2L)drm-P1 = Df(2L)drm-P2.