In contrast, ectopic expression of Wg alone induces Senseless expression in Wg-expressing and non-expressing cells where there is a lack of Notch activity (Figure 3D').
Using multigenerational selection experiments, we find that for the Drosophila proneural network, the effect of genomic diversity is dampened by miR-9a-mediated regulation of senseless expression.
Conversely, knockdown of Mad with RNAi (see below) caused decreased Senseless expression within clones (Figure 2H and 2I), which were accompanied in the adult wing by losses of the anterior wing margin within clones (Figure 2U).
Occasionally, we detected that f00391 was able to induce the Senseless expression defect even in wild-type eye discs (data not shown).
ELAV and Senseless expression patterns demonstrate that the hyperactivation of Psc leads to the same differentiation defects observed in the rbf1 120a;f00391 eye discs.
Although GMR-Gal4;failed failed to recapitulate the defect observed with ELAV staining, the same Senseless expression defect could be observed when Psc was overexpressed with GMR-Gal4.
Nevertheless, Psc overexpression produced a plethora of developmental defects that ranged from ectopic cell death to failure to maintain Senseless expression in R8 cells.
Moreover, the Senseless expression defect caused by Psc overexpression was not observed in the Caf1p55 mutant study by Anderson et al. indicating that Psc overexpression may have differential effects on CAF1p55-associated complexes or CAF1p55-independent effects.
Interestingly, unlike rbf1 120a eye discs overexpressing PSC, rbf1 120a;Caf1p55 long double-mutant eye discs did not show any effects on cell death, nor did they have defects in Senseless expression (data not shown).
However, despite its effect on cell death, Caf1p180 i did not suppress the f00391-induced ommatidial disorganization or the defect in Senseless expression, indicating that factors other than CAF1p180 are likely responsible for the sensitivity of rbf1 120a eyes to Psc-induced differentiation defects.
