dorsal cluster neuron & neurite
ventral adult lateral neuron & commissure
The mushroom body α-lobe morphological defects characteristic for Fmr1Δ113M homozygous adults are ameliorated by combination with a single copy of Nab2ex3, whereas the reverse is true for Nab2ex3 homozygotes in which the combination with one copy of Fmr1Δ113M further worsens the α-lobe phenotype. The β-lobe fusion observed in either of the two homozygous mutants cannot be modified by heterozygosity of the other gene's allele.
The eye defects (reduced size, partial depigmentation and disorganization of the ommatidial lattice) observed in adult flies expressing Nab2EP3716 under the control of Scer\GAL4GMR.PU can be suppressed by combination with a single copy of Fmr1Δ113M, while this worsens the locomotion deficit (decreased climbing ability) of adult flies expressing Nab2GD11745 controlled by Scer\GAL4elav-C155.
witA12/+ significantly suppresses the increases in mature boutons and branch number seen at the neuromuscular junction of Fmr1Δ113M/+ third instar larvae (though bouton and branch number is significantly higher in Fmr1Δ113M/+;witA12/+ larvae than witA12/+ larvae). witA12/witB11 fully suppresses the increase in mature boutons and branch number seen at the neuromuscular junction of Fmr1Δ113M/+ third instar larvae (branch number is significantly higher in witA12/witB11 larvae than Fmr1Δ113M/+;witA12/witB11 larvae).
The following defects associated with Fmr1Δ113M are suppressed by aubsting-1 heterozygosity: the near lethality of Fmr1Δ113M homozygotes; the sterility of Fmr1Δ50M/Fmr1Δ113M transheterozygous males and the fertility defects of Fmr1Δ113M heterozygous or homozygous males and females; the crystalline aggregates observed in the spermatocytes of Fmr1Δ113M heterozygotes and homozygotes; and the increased length of third instar larval neuromuscular junctions of Fmr1Δ113M homozygotes.
The crystalline aggregates observed in the spermatocytes of Fmr1Δ113M heterozygotes are also suppressed by the expression of aubScer\UAS.cBa under the control of Scer\GAL4nos.PU, Scer\GAL4T76, Scer\GAL4c135 or Scer\GAL4upd1.PU, but not by heterozygosity for aubHN2 or aubQC42, nor by the combination of aubHN2 heterozygosity and expression of aubScer\UAS.cBa under the control of Scer\GAL4upd1.PU.
rin2 Fmr1Δ113M double mutant eyes, generated by eyFLP/FRT-mediated mitotic recombination, show an increase in ommatidial number under normal food conditions. (Double mutants raised on food with reduced yeast content display eyes with a constant increase in ommatidial number, while mutants raised on increased yeast content show more pronounced variability in ommatidial number.) This phenotype is rescued to a rin2 like phenotype by inclusion of Fmr1+t14, and to a Fmr1Δ113M-like phenotype by inclusion of rin+t11.8, while rinT:Disc\RFP-mCherry does not completely rescue to a Fmr1Δ113M-like phenotype.
Animals with eyes overexpressing CaprKK100145 in a Fmr1Δ113M rin2 background, generated using the eyFLP Actin-Flp out-Gal4 system, results in late pupal lethality, with strongly overgrown eye/head structures visible in the pharates.
4.6% of ban12/Fmr1Δ113M transheterozygous adult females are fertile. ban12/Fmr1Δ113M double heterozygous adult females display a significant increase in the number of germaria with one or no germline stem cells, compared to controls, that progressively worsens from day 2 post-eclosion to day 12.
27% of Fmr1Δ113M/+; Dp(2;2)C619/+ double heterozygote brains show an ectopic collateral branch on the small LNv projections, while this phenotype is not seen in either single heterozygote. The posterior tract defasciculation phenotype phenotype is enhanced to a 91% penetrance in Fmr1Δ113M/+; Dp(2;2)C619/+ brains; the extent of defasciculation is greater in the double mutants and runs the entire length of the commissure. The penetrance of the increased LNv dorso-ventral and medio-lateral extension phenotype is higher in Fmr1Δ113M/+; Dp(2;2)C619/+ brains than in Fmr1Δ113M/+ brains. The penetrance of the LNv ectopic branch phenotype is increased to 100% and the posterior tract defasciculation phenotype is increased to 93% when Fmr1Δ113M/+ flies are also heterozygous for Rac1J11. The increased LNv dorso-ventral and medio-lateral extension phenotype is suppressed in Fmr1Δ113M brains that also carry a chic221/+ mutation.
The expression of Fmr1Scer\UAS.cZa under the control of Scer\GAL4T76 rescues the lethality of Fmr1Δ113M homozygotes and suppresses the crystalline aggregates observed in the spermatocytes of Fmr1Δ113M homozygotes and heterozygotes; this expression also partially rescues the male sterility of Fmr1Δ50M/Fmr1Δ113M transheterozygotes, and partially rescues the decreased fertilities of Fmr1Δ50M/Fmr1Δ113M transheterozygous females.
The expression of Fmr1Scer\UAS.cZa under the control of Scer\GAL4c135, Scer\GAL4nos.PU, or Scer\GAL4upd1.PU suppresses the crystalline aggregates observed in the spermatocytes of Fmr1Δ113M heterozygotes.