Fig. 1. perd is expressed in a subset of muscle founder cells (FCs) and is required for proper muscle development. (A) Double-labeling of a stage 12 wild-type embryo for perd RNA (blue) and Kruppel (Kr; brown) protein (which marks a subset of FCs) shows coexpression in some (arrows) but not all (arrowheads) Kr-positive FCs. (B) A high-magnification view of a stage 15 embryo shows that perd RNA is present in the muscle (arrows) and not in the tendon cell (bracket). (C-F) In contrast to injection of inactive control lacZ dsRNA (C,D), injection of double-stranded RNA corresponding to a portion of the perd gene (E,F) into embryos expressing tau-GFP in the somatic musculature causes specific muscles to develop with a rounded morphology and incorrect attachments (arrows), while other muscle groups are unaffected (arrowhead). (G) perd encodes a single-pass transmembrane protein of 2355 amino acids with two laminin G domains near its amino terminus and a carboxyl-terminal class II PDZ-binding motif (NQYWV). Asterisks indicate the positions of nonsense mutations in the EMS-induced alleles H2-5 (1), F1-3 (2), F2-5 (3) and 187(C2) (4). indicates the position of a four-nucleotide deletion in H1-4, resulting in a frameshift and early termination. (H,I) Immunostaining for myosin heavy chain shows that genetic loss of perd function causes the same muscle phenotype as RNAi, in which ventral longitudinal and segment border muscles have a rounded or teardrop shape (arrows), whereas lateral transverse muscles are normal (arrowhead).