Fig 9. CAP mutants show local disruptions of adult heart morphology.

Stacks of optical sections of adult hearts costained by F-actin/phalloidin and ßPS1-Integrin antibodies. (a, b) low magnification view of a w¹¹¹⁸ control heart stained for (a) F-actin by phalloidin (red) and (b) ßPS1-Integrin (green). (c, d) low magnification view of a CAP^42b heart stained for (c) F-actin and (d) ßPS1-Integrin; note disruptions indicated by local accumulation of actin fibers and clusters of Integrin (white arrows in c and d, respectively); bar 8 μm. (e-m) higher magnification view of heart regions stained for F-actin (f, i, l) and anti-ßPS1-Integrin (g, j, m); (e, h, k) merge. (e-g) shows a projection of an image stack for the w¹¹¹⁸ control with regularly arranged circular myofibrils (f; F-actin) that appear to smoothly continue across the line of contact sites of contralateral cells (open arrow in e and g; ßPS1-Integrin). (h-m) shows two consecutive projections of image stacks of a CAP^42b heart with cytological defects: (i, l) Disorganized cell contacts indicated by unorganized local masses and clustering of actin fibers (yellow arrowheads in l). Myofibrils in this region often do not contact the cell contact site and/or fold back into the cell interior (white arrows in l); (j, m) discontinuous, patchy organization of ßPS1-Integrin at cell contact sites (white arrowheads in m). (k) Unorganized actin masses and Integrin patches often colocalize (white and yellow arrowheads). bar: 8 μm.