The held out wing phenotype is enhanced from 2% penetrance in osa2/+ single mutants to 65% in Df(2R)ED3921/+; osa2/+ flies and 100% in Df(2R)ED3921; osa2/+ flies. The wing vein phenotype of Df(2R)ED3921 single mutants is enhanced by osa2, resulting in loss of L5 up to the posterior crossvein. The osa2 mutation causes an 87% suppression of the AntpNs homeotic transformation.
10+/-2% of KrIf-1/+ flies born to osa2/+ mothers have outgrowths with ectopic vibrissae protruding from the ventral region of the eye, compared to less than 0.1% of KrIf-1/+ flies born to isogenised wild-type mothers.
brm2 osa2 double heterozygotes have held-out wings in 97% of cases, a phenotype which is rarely seen in either single heterozygote. Antp73b/+ flies show transformation of antenna to leg. This phenotype is not suppressed by one copy of osa2. AntpNs/+ flies show transformation of antenna to leg. This phenotype is significantly suppressed by one copy of osa2. Expression of Antphs.PHTA during the larval stages results in antenna to leg transformations. This phenotype is not affected if the animals are also carrying osa2.