Flies homozygous for nmoP1 show ommatidia arrested at around 45[o] of rotation. The rate of rotation appears to be lower in these mutants compared to wild-type.
nmoP1 mutant flies exhibit wings that are smaller than wild-type and display a more rounded morphology and a held-out phenotype. Eyes are externally rough and narrower than wild-type. Tangential sections of those eyes reveal a high number of under-rotated ommatidia with a mean orientation angle of 59.3[o] with respect to the equator.
nmoP1 mutant eye discs display ommatidial rotation that is slower than in wild-type and that stop rotating prematurely. Apical shape change in the interommatidial cells, along with changes in cell area, are less evident in nmoP1 discs than in controls. The cone cell precursors also display abnormal behavior, with these cells being significantly more static in mutants than in controls.
Mutant ommatidia show reduced rotation of ommatidia compared to controls.
nmoP1/Df(3L)Exel6279 adults exhibit shorter circadian period of locomotor activity rhythms under constant darkness compared to controls.
Most neuromuscular junctions (NMJs) at muscles 6 and 7 lack branches containing more than five boutons in nmoP1/Df(3L)Exel6279 third instar larvae. There is a strong reduction in the number of type I synaptic boutons at muscles 6 and 7 and in the number of boutons at muscle 4 NMJs in the mutant larvae compared to wild type.
The number of boutons per muscle surface area is reduced at the neuromuscular junction in nmoP1/Df(3L)Exel6279, nmoP1/Df(3L)pbl-X1 and nmoDB24/nmoP1 third instar larvae.
Mutant ommatidial precursors rotate at a slower rate than wild-type ommatidial precursors in the developing eye. Initiation of ommatidial rotation and the first approximately 7[o] of rotation occurs normally in the mutant eye disc, but the average angle of rotation is significantly lower in the mutant eye discs than in wild-type from ommatidial row 5 onwards. The mutant ommatidia stall at 45[o] of rotation in the mutant eye disc, although in adults the average angle of rotation is 61[o] +/- 23 in mutant eyes.
No ectopic wing margin bristles are seen in nmoP1 mutant wings.
Ommatidia are arrested at approximately 45o to the equator.
nmoP1 heterozygous flies (genetic background = Canton-S) have a small but significant decrease in geotaxis score compared to wild-type (Canton-S) flies.
nmoP1/nmoadk2 flies have a smaller eye than normal in which the ommatidia are square instead of the normal hexagonal shape and are generally flanked by 4 interommatidial bristles (instead of the usual 3 bristles at alternating corners). Slight extra vein material near the posterior crossvein is seen in a small percentage of nmoP1 flies. Flies do not show any noticeable polarity defects in the wing.
Eyes of nmo mutant flies are slightly narrowed anterior-posterior, and the facets are square rather than hexagonal. Pigment cell lattice is abnormal, especially at the corners, which have disarranged bristle and secondary pigment cells. Occasionally ommatidia are fused three to ten per eye. Most ommatidia have normal numbers of photoreceptor cells, although some lack a few. Viability is reduced to 10% of wild type and the angle of wings is 15o to 30o. In mutant eye discs the 5 cell precluster completes its first 45o rotation, but does not continue to the full 90o rotation. This also applies to the cone cells and primary pigment cells.
nmoP1/Df(3L)Exel6279 has abnormal locomotor rhythm phenotype, enhanceable by ClkS859A.Tag:V5/Clkout
nmoP1 has abnormal planar polarity phenotype, enhanceable by Vangstbm-6
nmoP1 has abnormal planar polarity phenotype, enhanceable by pksple-1
nmoP1/Df(3L)Exel6279 has abnormal locomotor rhythm phenotype, non-enhanceable by Clkout/ClkTag:V5.WT
nmoP1 has abnormal cell polarity phenotype, non-enhanceable by KrnUAS.cUa/Scer\GAL4sev.EP
nmoP1 has abnormal cell polarity phenotype, non-enhanceable by ru1
nmoP1/Df(3L)Exel6279 has abnormal locomotor rhythm phenotype, non-suppressible by Clkout/ClkTag:V5.WT
nmoP1 has abnormal cell polarity phenotype, non-suppressible by ru1
nmoP1 has abnormal cell polarity phenotype, non-suppressible by KrnUAS.cUa/Scer\GAL4sev.EP
nmoj147-1/nmoP1 has abnormal planar polarity phenotype, non-suppressible by hhbar3/hhbar3
nmoP1/nmo[+] is an enhancer of visible phenotype of Scer\GAL4dpp.blk1, tkvQ253D.UAS.cNb
nmoP1 is a non-enhancer of abnormal planar polarity | adult stage phenotype of FrlDN.UAS, Scer\GAL4sev.EP
nmoP1/nmo[+] is a non-enhancer of abnormal cell polarity phenotype of Scer\GAL4hs.2sev, shgdCR3h.UAS.sgGFP
nmoP1 is a suppressor of abnormal cell polarity phenotype of aosrlt
nmoP1/nmo[+] is a non-suppressor of abnormal cell polarity phenotype of Scer\GAL4hs.2sev, shgdCR3h.UAS.sgGFP
Madk00237/Mad[+], nmoP1 has abnormal neuroanatomy | dominant | third instar larval stage phenotype
Mad[+]/Mad6, nmoP1 has abnormal neuroanatomy | dominant | third instar larval stage phenotype
dgo308, nmoP1 has partially lethal - majority die phenotype
nmoP1 has ommatidium phenotype, enhanceable by Vangstbm-6
nmoP1 has ommatidium phenotype, enhanceable by pksple-1
nmoP1 has ommatidium phenotype, non-enhanceable by KrnUAS.cUa/Scer\GAL4sev.EP
nmoP1 has ommatidium phenotype, non-enhanceable by ru1
nmoP1 has eye phenotype, non-enhanceable by a7/Df(2R)aEX1
nmoP1 has ommatidium phenotype, non-suppressible by KrnUAS.cUa/Scer\GAL4sev.EP
nmoP1 has ommatidium phenotype, non-suppressible by ru1
nmoj147-1/nmoP1 has ommatidium phenotype, non-suppressible by hhbar3/hhbar3
nmoP1 has eye phenotype, non-suppressible by a7/Df(2R)aEX1
nmoP1/nmo[+] is an enhancer of anterior wing margin phenotype of Pknk06808
nmoP1 is an enhancer of eye phenotype of Scer\GAL4hs.2sev, miple1UAS.Tag:HA
nmoP1 is an enhancer of ommatidium phenotype of Scer\GAL4hs.2sev, miple1UAS.Tag:HA
nmoP1 is an enhancer of eye phenotype of Scer\GAL4GMR.PU, miple1UAS.Tag:HA
nmoP1 is an enhancer of ommatidium phenotype of Scer\GAL4GMR.PU, miple1UAS.Tag:HA
nmoP1 is an enhancer of wing margin bristle | ectopic phenotype of dgo308
nmoP1/nmo[+] is an enhancer of wing blade phenotype of Scer\GAL4dpp.blk1, tkvQ253D.UAS.cNb
nmoP1 is a non-enhancer of ommatidium phenotype of FrlDN.UAS, Scer\GAL4sev.EP
nmoP1/nmo[+] is a non-enhancer of ommatidium phenotype of Scer\GAL4hs.2sev, shgdCR3h.UAS.sgGFP
nmoP1/nmoP1 is a non-enhancer of eye phenotype of a7/Df(2R)aEX1
nmoP1 is a suppressor of ommatidium phenotype of aosrlt
nmoP1/nmo[+] is a non-suppressor of ommatidium phenotype of Scer\GAL4hs.2sev, shgdCR3h.UAS.sgGFP
nmoP1/nmoP1 is a non-suppressor of eye phenotype of a7/Df(2R)aEX1
Madk00237/Mad[+], nmoP1 has NMJ bouton | third instar larval stage phenotype
Mad[+]/Mad6, nmoP1 has NMJ bouton | third instar larval stage phenotype
Presence of nmoP1 does not significantly alter eye phenotypes seen in flies with FrlDN.Scer\UAS driven by Scer\GAL4sev.EP.
Expression of ClkT:SV5\V5.WT (in a Clkout mutant background) does not alter the locomotor rhythm defects seen in nmoP1/Df(3L)Exel6279.
Expression of ClkS859A.T:SV5\V5 (in a Clkout mutant background) enhances the locomotor activity rhythm defects seen in nmoP1/Df(3L)Exel6279 mutants.
A nmoP1 mutant background enhances the ommatidial rotation phenotype seen in flies expressing miple1Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4hs.2sev.
Dosage reduction of nmo, through a nmoP1 mutant background is able to enhance the eye roughness seen in Scer\GAL4GMR.PU>miple1Scer\UAS.T:Ivir\HA1 mutants.
Many ommatidia do not rotate at all and remain oriented parallel to the equator in Vangstbm-6 nmoP1 and in pksple-1 nmoP1 double mutants.
The penetrance of the bifurcated wing phenotype caused by expression of tkvQ253D.Scer\UAS.cNb under the control of Scer\GAL4dpp.blk1 is enhanced by nmoP1/+ from 20.8% to 86.3%.
A nmoP1/+ background does not affect the Scer\GAL4hs.2sev>shgdCR3h.Scer\UAS.T:Avic\GFP-rs ommatidial phenotype.
KrnScer\UAS.cUa, (driven by Scer\GAL4sev.EP) or ru1 has no effect on the nmoP1 ommatidial phenotype.
Has no effect on the eye phenotype produced by activated arm constructs. (either armS44Y.GMR or armS56F.GMR).
The addition of nmoP1/nmoP1 has no effect on a7/Df(2R)aEX1 flies.
nmoP1/nmoDB is rescued by nmoII.tub.GFP
nmoP1/Df(3L)Exel6279 is rescued by Scer\GAL4tim.PU/nmoUAS.cUa.GFP
nmoP1/Df(3L)Exel6279 is rescued by Scer\GAL4unspecified/nmoUAS.cUa.GFP
nmoP1 is partially rescued by nmoUAS.cUa/Scer\GAL4ct.PB
nmoP1/nmoDB is partially rescued by nmoUAS.cUa/Scer\GAL4hs.2sev
nmoP1 is partially rescued by nmoI.UAS.EGFP/Scer\GAL4hs.2sev
nmoP1 is partially rescued by nmoII.UAS.EGFP/Scer\GAL4hs.2sev
nmoP1/Df(3L)Exel6279 is not rescued by Scer\GAL4G14/nmoUAS.cUa.GFP
Expression of nmoScer\UAS.cUa under the control of Scer\GAL4ct.PB in a nmoP1 homozygous background rescues the reduction in ommatidial rotation angle, with the percentage of ommatidia rotating over 50[o] significantly higher than in nmoP1 mutants.
The reduced number of boutons per muscle surface area seen at the neuromuscular junction in nmoP1/Df(3L)Exel6279 is rescued by neuronal expression of nmoScer\UAS.cUa.T:Avic\GFP under the control of Scer\GAL4unspecified but not by expression of nmoScer\UAS.cUa.T:Avic\GFP under the control of Scer\GAL4G14.
Expression of nmoII.Scer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL4hs.2sev partially rescues the nmoP1 ommatidial rotation defect (in all 3 insertion lines tested).
Expression of nmoI.Scer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL4hs.2sev results in inconsistent rescue of the nmoP1 ommatidial rotation defect (partial rescue is seen in 2 insertion lines, while one line almost completely rescues the defect).
Δ2-3 induced reversion of the mutant phenotype is accompanied by loss of the P-element from nmoP1. nmo mutants are epistatic to argosrlt with respect to ommatidial precluster orientation.