Amino acid replacement: K45N. K45N falls in the basic region of the bHLH region. Nucleotide substitution: A404C (nucleotide positions as in cDNA sequence of FBrf0056120).
A8231686C
A404C
K45N | dpn-PA
K45N
neuroblast MBp | larval stage (with dpn1)
type II neuroblast | larval stage (with dpn1)
Type II neuroblasts are completely absent in the brains of late third larval instar dpn1/dpn7 larvae. The number of type I neuroblasts is close to that of wild type at 9-12 hours after larval hatching (ALH), but is reduced compared to wild type at 48 hours ALH, and does not reduce further from 48 hours to 96 hours ALH.
Mushroom body neuroblasts are progressively lost in dpn1/dpn7 mutants: at the late third instar larval stage nearly half of the mushroom body neuroblasts are missing, and by the start of pupariation, 90% of them are lost.
Homozygous mushroom body neuroblast clones generated immediately after larval hatching have mostly lost their neuroblasts by 1-2 days after pupariation, in contrast to wild-type control clones, which always contain a neuroblast at this stage.
Heterozygous larvae show a slight decrease in the number of type II neuroblasts in the brain compared to wild type.
The few Df(2R)dpn-2/dpn7 mutant escapers that are seen are uncoordinated and flightless. The total number of neuroblasts is reduced during the larval stages. Type II neuroblasts are never observed at late stages of larval development although one is occasionally seen in early larval brains.
dpn7 mutant clones generated in type II neuroblasts are smaller than control clones. In contrast, clones that originate in type I clones are similar in size to controls.
Strongly feminizes triploid intersexes. Degree of feminization of the foreleg is unusually high (35% of forelegs are entirely female). May be cell lethal in germ-line clones.
dpn7/dpn1 has abnormal neuroanatomy | third instar larval stage phenotype, suppressible | partially by pros[+]/prosV17
dpn7 is a non-suppressor of abnormal neuroanatomy | somatic clone | third instar larval stage phenotype of Nint.G.UAS, Scer\GAL4αTub84B.PL
dpn7 is a non-suppressor of increased cell number | somatic clone | third instar larval stage phenotype of Nint.G.UAS, Scer\GAL4αTub84B.PL
dpn7 has type II neuroblast | larval stage phenotype, non-enhanceable by N[+]/N55e11
dpn7/dpn1 has type I neuroblast | third instar larval stage phenotype, suppressible | partially by pros[+]/prosV17
dpn7 has type II neuroblast | larval stage phenotype, non-suppressible by N[+]/N55e11
dpn7 is a non-suppressor of type II neuroblast | ectopic | somatic clone | third instar larval stage phenotype of Nint.G.UAS, Scer\GAL4αTub84B.PL
prosV17/+ partially rescues the reduction in number of type I neuroblasts which is seen in the brains of late third larval instar dpn1/dpn7 larvae.
The decrease in the number of type II neuroblasts in the brain that is seen in dpn7/+ larvae is unaffected if the animals are also heterozygous for N55e11.
dpn7 does not suppress the ectopic neuroblast phenotype seen when clones expressing Nint.G.Scer\UAS are induced under the control of Scer\GAL4αTub84B.PL.
Shows complex complementation behavior. Complementation between mutant dpn alleles reveals differences in strength but little male-specific lethality.