(Downloading may take up to 30 seconds.
If the slide opens in your browser, select File -> Save As to save it.)
Click on image to view larger version.



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-Rac7A/+, (C) GMR-Rac7A/DMYPT03802, (D) RhoA720/+;GMR-Rac7A/+, (E) Drok2/+;GMR-Rac7A/+, (F) zip1/+;GMR-Rac7A/+, (G) ckP13/+;GMR-Rac7A/+ and (H) sqh[A20A21]/+;GMR-Rac7A/+.