Fig. 7.

Injection of ca-AKT1 in rgs4 morphants could not rescue axonal defects in the hindbrain. a Defects such as failure of Mauthner axons to cross each other at the midline and fewer acetylated α-tubulin stained commissural axons could be detected in Rgs4 knockdown embryos, and neither of these phenotypes could be restored by injection of constitutively-activated AKT1. b Quantification confirms number of embryos with aberrant Mauthner axon trajectory are significantly increased in either rgs4 morphants or embryos coinjected with rgs4 morpholino and constitutively-activated AKT1. c Quantification of axons indicates significant loss of hindbrain commissural axons in rgs4 morpholino-injected embryos, and injection of constitutively-activated AKT1 failed to restore the hindbrain phenotypes. ca-AKT1, constitutively-activated AKT1; rgs4 MO, rgs4 morpholino. *p < 0.05; ***p < 0.001