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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).
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