Polytene chromosomes normal.
100% of homozygotes lack the posterior crossveins.
No obvious tergal depressor of trochanter (TDT) muscle fiber defect is observed in homozygous cv-21 animals.
Mutant larvae do not have defects in the establishment or maintenance of dendritic tiling in class IV dendrite arborisation (da) neurons.
Mutants lack crossveins.
cv-21 in combination with Df(2R)Pu-D17 always leads to the loss of the posterior crossvein (PCV) and can lead to the loss of the whole of the anterior crossvein (ACV) and the ends of some longitudinal veins. Homozygotes lack most or all of the PCV and in some cases the posterior of the ACV.
Anterior and posterior crossveins absent. RK1.
cv-21 has visible phenotype, suppressible by ltlUAS.cSa
cv-21 has posterior crossvein phenotype, suppressible by ltlUAS.cSa
cv-21 has crossvein phenotype, suppressible by ash2S112411
cv-21 is a non-suppressor of crossvein | ectopic phenotype of ash2S112411
Two copies of P{UAS-ltl.S}5 (which allow leaky expression of ltlScer\UAS.cSa in the absence of a Scer\GAL4 driver) fully restore the posterior crossvein in 45% of wings of cv-21/cv-21 animals.
cv-21/cv-21, ash2S112411/+ flies have normal crossveins. cv-21/cv-21, ash2S112411/ash2S112411 have extra crossveins and reduction in wing size.
cv-21 is rescued by Scer\GAL4A9/cv-2UAS.cSa
Expression of one copy of cv-2Scer\UAS.cSa under the control of Scer\GAL4A9 rescues the posterior crossvein defects seen in homozygous cv-21 mutants.
Expression of cv-2N.Scer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL4hh.PU partially rescues the rescues the posterior crossvein defects seen in homozygous cv-21 mutants.
Segregated from: Several natural populations.
