Homozygous embryos lack many of the dorsal and ventral somatic muscles. The expressivity of the phenotype varies for each muscle and not all muscles are affected. Muscle DA1 is almost always absent, while muscle DO1 is lost from more than 50% of hemisegments. The number of eve-expressing pericardial cells is increased compared to wild-type. The founder cell of the DA1 muscle (FDA1) and its sibling (FDA1sib) both adopt an FDA1sib-like identity. The sibling of the founder cell of the DO1 muscle (FDO1sib) is duplicated at the expense of the founder cell of the DO1 muscle (FDO1). numb3 inscP49 embryos have a qualitatively similar phenotype to numb3 embryos, although they exhibit these phenotypes at higher expressivity.
Clonal analysis revealed an adult mutant macrochaetae phenotype of extra sockets at the expense of hair cells in the notum. Microchaetae in mutant patches show a broader spectrum of transformations, some with a remnant of a hair cell associated with multiple socket-like cells.
apparently null since the neuronal phenotype of homozygotes is indistinguishable from that of hemizygotes.
Df(3R)Exel6157/+, numb3 has cardiogenic mesoderm phenotype
Df(1)CHES-1-like1/+, numb3 has cardiogenic mesoderm phenotype
numb3/+ ; Df(3R)Exel6157/+ double heterozygous embryos show asymmetric cell division defects in "svp" cardiac progenitor cells that are significantly more severe than the additive effects of each of the two single heterozygotes. Defects in the symmetric cell divisions that give rise to the tin-expressing cardial cells in the double heterozygotes are not significantly different from the additive effects of each of the two single heterozygotes.
numb3/+ ; Df(1)CHES-1-like1/+ double heterozygous embryos show asymmetric cell division defects in "svp" cardiac progenitor cells that are significantly more severe than the additive effects of each of the two single heterozygotes. Defects in the symmetric cell divisions that give rise to the tin-expressing cardial cells in the double heterozygotes are not significantly different from the additive effects of each of the two single heterozygotes.
On the basis of CNS phenotype numb alleles form a series: numb2 > numb4 > numb1/numb3.