F-actin accumulation in <i>hid-p35</i> clones depends on LIMK1 and Cofilin, but not JNK signaling.

(A-J’) Late 3rd instar wing discs with 48-hour old mosaic clones positively marked by GFP. Phalloidin (PHN, magenta in A-J and grey in A’-J’) labels F-actin. Images of the apical side of the discs are shown in A, C and E-J. B and D show the cross sections corresponding to the yellow lines indicated in A and C, respectively. The apical (a) and basal (b) surfaces of these cross sections are as indicated. Compared to the control clones expressing P35 only (A-B’), simultaneous expression of hid and p35 (hid-p35 clones) leads to an accumulation of F-actin apically in the clones (arrows in C, C’ and clones highlighted by yellow dotted lines in D, D’). This F-actin accumulation in hid-p35 clones is suppressed by expression of droncRNAi (E, E’), LIMK1RNAi (F, F’) or in LIMK12 hemizygous mutants (G, G’). Expression of cofilin in the hid-p35 clones further reduces the level of F-actin (H, H’). In contrast, F-actin accumulation persists the hid-p35 clones with expression of a dominant negative mutant of bsk (bskDN, I, I’, arrows) or in a Tak1 hemizygous null mutant background (J, J’, arrows). (K) Quantification of the F-actin signal intensity in the representative clones of the indicated genotypes in the wing disc pouches. Images of the apical side of the discs were used. Compared to the p35 clones, the DHE signals are significantly (****p hid-p35 clones. This increase is significantly (****p SOD, cofilin or in LIMK12 mutants. In contrast, expression of bskDN or DuoxRNAi has no significant (n.s.) effects.