Imprecise excision of P{SUPor-P}MAN1KG06361 generated a deletion from position +1437 relative to the transcription start site that extends to +2117, with 321bp of the P-element remaining at the initial insertion site. This removes the C-terminal Mad-binding domain.
Approximate endpoints of a deletion resulting from the imprecise excison of P{SUPor-P}MAN1KG06361, that is reported as extending from +1437 to +2117 relative to the MAN1 transcription start site. It's not clear what coordinate was used as the TSS.
MAN1ΔC mutants show no detectable effects in nuclear envelope formation.
Approximately 28% of the expected MAN1ΔC homozygous adults do not emerge. The eclosed adults show a decreased life span, male sterility and decreased female fertility when compared to wild-type flies.
MAN1ΔC mutants are also flightless.
While more than 90% of the wild-type and MAN1ΔC heterozygotes reach 10 cm in 20 seconds, only 30-35% of the MAN1ΔC homozygotes are able to reach the mark in the same time, suggesting that the motor ability of MAN1ΔC mutants is impaired.
There are no obvious phenotypes in muscle size, positioning and fibrillar composition in body wall muscle preparations from MAN1ΔC instar larvae. There are no defects in the major thoracic indirect flight muscles. There are no defects in embryonic axon guidance. All motoneurons appear to have established contact with their appropriate targets and synaptic morphology appears unaffected in MAN1ΔC mutant larvae.
The amplitude of nerve-evoked excitatory post-synaptic currents (eEPSC) in MAN1ΔC is reduced to 27% of wild-type levels. The amplitude of spontaneous miniature excitatory post-synaptic currents (mEPSCs) in response to single vesicle fusion events is not altered. The impaired synaptic transmission in MAN1ΔC mutants is caused by a decrease in quantal content. There are no significant changes in rise time and decay time constants of eEPSCs or mEPSCs, indicating that the time course of vesicle release and receptor desensitization kinetics are not severely affected.
MAN1ΔC adults exhibit ectopic vein tissue emanating from the posterior cross vein. No defects in the size of the wing blade or the distance between the LVs. The ectopic venation shows incomplete penetrance, with 87% of the mutant female individuals showing additional vein material at one or both wings. Ectopic venation is less prominent in MAN1ΔC males (30-40%), probably due to differences in wing size.
MAN1ΔC has posterior crossvein phenotype, suppressible by dpps11/dpp[+]
MAN1ΔC has posterior crossvein phenotype, suppressible by gbb1/gbb[+]
MAN1ΔC is rescued by Scer\GAL4Act5C.PI/MAN1UAS.cWa
MAN1ΔC is partially rescued by Scer\GAL4elav-C155/MAN1UAS.cWa
MAN1ΔC is partially rescued by Scer\GAL4Mef2.PR/MAN1UAS.cWa
MAN1ΔC is partially rescued by MAN1UAS.cWa
The climbing defect of MAN1ΔC flies can be rescued by expression of MAN1Scer\UAS.cWa under the ubiquitous Scer\GAL4Act5C.PI driver.
Expression of MAN1Scer\UAS.cWa within the presynaptic motoneuron, using the neuronal driver Scer\GAL4elav-C155 or within the post-synaptic muscle with the Scer\GAL4Mef2.PR driver is not sufficient to fully restore motor ability.
Partial rescue of MAN1ΔC mutants is observed through the introduction of one or two copies of MAN1Scer\UAS.cWa without a Scer\GAL4 driver. Both motor ability and synaptic phenotypes are partially rescued.
Both the pre- and post-synaptic expression of MAN1Scer\UAS.cWa (under the control of Scer\GAL4Mef2.PR or Scer\GAL4elav-C155 can partially rescue the drop in EPSC amplitude detected in MAN1ΔC larvae.
The low eEPSC amplitude of MAN1ΔC mutants is increased dramatically in mutants carrying a single copy of gbb1.
