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Fig. 6 | Cell Communication and Signaling

Fig. 6

From: Abelson kinase’s intrinsically disordered region plays essential roles in protein function and protein stability

Fig. 6

Abl∆IDR does not rescue defects leading edge cell shape. Leading edge, stage 13–14 embryos, anterior left, dorsal up unless noted, stained with antibodies to Ecad to visualize cell shapes. a Wildtype. The leading edge is straight, with even cell widths at the leading edge (blue arrows), excepting the slightly increased width at the positions of segmental grooves (red arrowheads). Scale bar = 10 µm. b Expressing Abl∆IDR in a wildtype background did not produce apparent defects in cell shape change during dorsal closure. c ablM/Z mutant, exhibiting the characteristic defects in leading edge cell shape. Leading edge cells are uneven in width, with some splayed open (magenta arrows) and some hyperconstricted (yellow arrows). Groups of cells also fail to elongate (red asterisks). d, e Representative Abl∆IDR; ablM/Z mutants. As in the unrescued mutant, leading edge cells are uneven in width, with some splayed open (magenta arrows) and some hyperconstricted (yellow arrows). Groups of cells also fail to elongate (red asterisks). f Abl∆IDR; ablM/Z mutant, dorsal view. Similar cell shape defects are seen in embryos that have completed or almost completed closure. g Abl∆IDR; ablM/Z mutant. Green asterisks indicate large, presumed multinucleate cells. h Abl∆CR1; ablM/Z mutant for comparison

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