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. 2008 Mar;178(3):1371–1383. doi: 10.1534/genetics.107.083808

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Copyright © 2008 by the Genetics Society of America

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Figure 3.— — Functional analysis of PDZ-domain binding motifs and conserved serines that are candidates for phosphorylation. (A) Schematic of the UAS-sns5xPDZ-HA and UAS-snsA17-HA transgenes. The mutated sites and their amino acid substitutions are indicated. (B–G) Lateral views of representative embryos in which the musculature has been visualized by immunostaining with an antibody to muscle myosin. (B–D) Expression of the transgene was directed by mef2Gal4 in a sns^Zf1.4/sns^XB3 mutant embryo, with individual transgenes: (B) UAS-sns-HA, (C) UAS-sns5xPDZ-HA, and (D) UAS-snsA17-HA. (E–G) Expression of the transgene was directed by snsGal4 in a sns^Zf1.4/sns^Zf1.4 mutant embryo, with individual transgenes: (E) UAS-sns-HA, (F) UAS-sns5xPDZ-HA, and (G) UAS-snsA17-HA. There is no apparent difference in the ability of full-length and mutagenized transgenes to rescue the myoblast fusion defect of sns mutants when driven by mef2Gal4 and snsGal4. Bar, 20 μm.