aCC and RP2 fail to exit the CNS in eveΔRP2A mutants.
eveΔRP2A mutants exhibit a failure of aCC/RP2 motoneurons to project out of the ventral nerve cord. In aCC, these effects are highly penetrant and observed at several stages, whereas in RP2 the effects are partially penetrant at stage 12 and almost absent at stage 15.
eveΔRP2A has abnormal neuroanatomy phenotype, enhanceable by unc-5[+]/beat-Ia[+]/unc-58/beat-Ia3
eveΔRP2A has abnormal neuroanatomy phenotype, enhanceable by unc-5[+]/unc-58
eveΔRP2A has abnormal neuroanatomy phenotype, enhanceable by beat-IaUAS.cFa/Scer\GAL4eve.RN2
eveΔRP2A has abnormal neuroanatomy phenotype, enhanceable by unc-5UAS.Tag:HA,Tag:SS(wg)/Scer\GAL4eve.RN2
eveΔRP2A has abnormal neuroanatomy phenotype, enhanceable by Scer\GAL4eve.RN2/Fas2UAS.cLa
eveΔRP2A has abnormal neuroanatomy phenotype, enhanceable by Nrg180.I.UAS/Scer\GAL4eve.RN2
eveΔRP2A has abnormal neuroanatomy phenotype, non-suppressible by Scer\GAL4eve.RN2/grnUAS.cBa
eveΔRP2A is an enhancer of abnormal neuroanatomy phenotype of Scer\GAL4eg-Mz360, unc-5UAS.Tag:HA,Tag:SS(wg)
eveΔRP2A, beat-Ia[+], eve[+], beat-Ia3 is an enhancer of abnormal neuroanatomy phenotype of unc-58
eveΔRP2A/eve[+] is an enhancer of abnormal neuroanatomy phenotype of unc-58
eveΔRP2A is an enhancer of abnormal neuroanatomy phenotype of Nrgl7
Scer\GAL4eve.RN2, beat-IaUAS.cFa, eveΔRP2A has abnormal neuroanatomy phenotype
Df(2R)eve, eveΔRP2A, unc-58 has abnormal neuroanatomy phenotype
eveΔRP2A has larval intersegmental nerve phenotype, enhanceable by unc-5[+]/beat-Ia[+]/unc-58/beat-Ia3
eveΔRP2A has larval VUM motor neuron phenotype, enhanceable by beat-IaUAS.cFa/Scer\GAL4eve.RN2
eveΔRP2A has larval VUM motor neuron phenotype, enhanceable by unc-5UAS.Tag:HA,Tag:SS(wg)/Scer\GAL4eve.RN2
eveΔRP2A has larval VUM motor neuron phenotype, enhanceable by Scer\GAL4eve.RN2/Fas2UAS.cLa
eveΔRP2A has larval VUM motor neuron phenotype, enhanceable by Nrg180.I.UAS/Scer\GAL4eve.RN2
eveΔRP2A has larval DA1 motor neuron phenotype, non-suppressible by Scer\GAL4eve.RN2/grnUAS.cBa
eveΔRP2A is an enhancer of larval VUM motor neuron phenotype of Scer\GAL4eg-Mz360, unc-5UAS.Tag:HA,Tag:SS(wg)
eveΔRP2A, beat-Ia[+], eve[+], beat-Ia3 is an enhancer of larval intersegmental nerve phenotype of unc-58
eveΔRP2A/eve[+] is an enhancer of larval intersegmental nerve phenotype of unc-58
eveΔRP2A is an enhancer of larval intersegmental nerve phenotype of Nrgl7
Scer\GAL4eve.RN2, beat-IaUAS.cFa, eveΔRP2A has larval VUM motor neuron phenotype
Df(2R)eve, eveΔRP2A, unc-58 has larval intersegmental nerve phenotype
A transheterozygous combination of eveΔRP2A/+, unc-58/+ reduces beat-Ia levels to 50% and significantly increases the defects seen in intersegmental nerves, with the number of axons exhibiting stalling increasing from 3% to 7.5% in eveΔRP2A/+, unc-58/+ transheterozygotes and eveΔRP2A/+, unc-58/+, beat-Ia3/+ triple heterozygotes, respectively.
Expression of unc-5Scer\UAS.T:Ivir\HA1,T:SS-wg in an eveΔRP2A mutant background results in 11% of hemisegments exhibiting dual motoneuron exit. These mutants exhibit an increase in dorsal projections in 67% of hemisegments.
Expression of beat-IaScer\UAS.cFa in an eveΔRP2A mutant background results in the exit of a single motoneuron of the pair in each hemisegment. These mutants exhibit an increase in dorsal projections in 36% of hemisegments.
Expression of Fas2Scer\UAS.cLa in an eveΔRP2A mutant background results in the exit of a single motoneuron of the pair in each hemisegment. These mutants exhibit an increase in dorsal projections in 25% of hemisegments.
Expression of Nrg180.I.Scer\UAS in an eveΔRP2A mutant background results in the exit of a single motoneuron of the pair in each hemisegment.
Removing one copy of eve in Nrgl7/Y mutants results in more severe intersegmental nerve guidance defects with a significant increase in axon stalling upon the addition of eveΔRP2A.
Expression of grnScer\UAS.cBa in the aCC/RP2 neurons, under the control of Scer\GAL4eve.RN2 does not rescue the failure of aCC to project its axon out of the ventral nerve cord in eveΔRP2A mutants.
eveΔRP2A partially rescues eveunspecified
Two copies of eveΔRP2A fully rescue segmentation function in eve null mutants. However, at the extended germband stage, eve expression in the mesoderm is often weak or missing.
Homozygous Df(2R)eve embryos carrying two copies of eveΔRP2A show defects in the RP2, aCC and pCC neurons.
eve null mutants carrying a copy of eveΔRP2A and eveΔRP2C in trans show normal mesodermal expression of eve and normal segmentation and are efficiently rescued to adulthood.