Amino acid replacement: Q185term.
The mutation is predicted to produce a truncated protein that lacks the POU (DNA binding) domain.
Nucleotide substitution: C?T.
C12684881T
C?T
Q185term | pdm2-PA; Q580term | pdm2-PB; Q580term | pdm2-PC; Q580term | pdm2-PD
Q185term
Lethal when heterozygous with Df(2L)prd1.7 and viable when heterozygous with Df(2L)Prl. Homozygotes exhibit defects in the formation of the RP2 motoneuron. Number of hemisegments with a mature RP2 neuron in homozygous embryos is reduced to 76%, loss of RP2 phenotype. The failure to produce mature RP2 neurons is attributable, at least in part, to GMC4-2a adopting an aberrant cell identity. Heterozygotes with Df(2L)pdm-2PR6 have only 80% of hemisegments with a mature RP2 neuron. P{HSpdm-1} can restore at least some of the mature RP2 motoneurons in pdm2E46/Df(2L)prd1.7 embryos, in which mature motoneurons are not made.