Fig. 2. Loss of PINCH function disrupts muscle morphology and actin filament organization. (A,B) Lateral views of stage 16 embryos stained with an antibody against the Mlp84B protein to visualize the somatic muscles. The stck mutant (B) displays a disruption in muscle fiber morphology. Arrowheads in B indicate areas where the muscles have lost their attachment to the tendon matrix. Arrows in A,B indicate enrichment of Mlp84B at muscle-attachment sites. (C-G) Confocal micrographs of embryonic muscle from wild-type (C,E), stck¹⁸/l(3)097 (D), stck¹⁷/l(3)097 (F) and l(3)097 homozygote (G) embryos, labeled with fluorescent-phalloidin to visualize F-actin. (C,D) Muscle fibers from early stage 17 embryos. A set of lateral muscles from two segments is shown in each panel. Actin bundles are readily distinguished in the wild-type muscles because of the precise orientation of the actin filaments in each muscle. This arrangement is not maintained in the mutant muscles (D). (E-G) Late stage 17 embryos. Note that the defects exhibited by a stck¹⁷/l(3)097 embryo (F) are similar to those from the l(3)097 homozygote (G), when compared with a wild-type embryo (E). Equivalent regions are indicated by an asterisk in the mutant and wild type.

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