Fig. 7. DMYPT is a negative regulator of Rho/myosin II signaling in vivo. Heterozygosities for loss-of-function mutations in RhoA (D), Drok (E), zip (F), and the non-phosphorylatable sqh mutation (H), suppress the rough eye phenotype caused by GMR-Rac (B). In contrast, loss-of-function mutations in DMYPT (C) and ck (G) enhance the GMR-Rac phenotype. (A) OreR (wild type, +), (B) GMR-Rac^7A/+, (C) GMR-Rac^7A/DMYPT⁰³⁸⁰², (D) RhoA⁷²⁰/+;GMR-Rac^7A/+, (E) Drok²/+;GMR-Rac^7A/+, (F) zip¹/+;GMR-Rac^7A/+, (G) ck^P13/+;GMR-Rac^7A/+ and (H) sqh[A20A21]/+;GMR-Rac^7A/+.

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