Fig. 2. Genetic interactions between SCF and the MSL complex. (A) Expression levels of MSL proteins and rox RNAs are not affected by knockdown of SCF. Control individuals (carrying only GAL4) and RNAi-induced individuals (carrying both GAL4 and UAS-IRscf) were sampled from third-instar male larvae. The expression levels of MSL-1, MSL-2, MSL-3, MLE, MOF and tubulin were examined by immunoblotting (left panel), and rox1 and rox2 RNA expression levels were analyzed by RT-PCR (right panel) with rp49 as a control. First-strand cDNA synthesized from each RNA sample was diluted (1:3, 1:9 and 1:27) and used as PCR template. (B) Effect of the scf deficiency on the survival of females expressing msl-2 under the control of a constitutive promoter. To generate the progeny females listed in the boxes, [H83MSL2]/+ males were crossed to scf/TM6B females (left) or [Hsp83-SCF];scf/TM6B females (right). Day 1 represents the day when the first population eclosed. Females bearing the [H83MSL2] transgene displayed developmental delay and decreased viability compared with their sisters lacking the transgene. The scf deficiency significantly rescued these females (left graph). Moreover, the rescue was suppressed by introducing Hsp83-driven scf cDNA (right graph).