Skip to main content
. Author manuscript; available in PMC: 2014 Dec 1.
Published in final edited form as: Dev Dyn. 2013 Oct 2;242(12):1466–1477. doi: 10.1002/dvdy.24059

Fig. 5. Knockdown of Aae comm2 results in a commissureless phenotype.

Fig. 5

Aae comm2 knockdown (KD) was confirmed through whole-mount in situ hybridization, which demonstrated that two siRNAs targeting comm2, siRNA-1 (B) and siRNA-2 (C), resulted in loss of comm2 transcripts throughout the entire embryo, including the nerve cord. comm2 levels were not noticeably altered by injection of control siRNA (A, arrow marks ventral nerve cord expression). Lateral views are shown in panels A–C which are oriented anterior left and ventral downward. In D–H, anti-acetylated tubulin staining marks the axons in the filleted ventral nerve cords (oriented anterior upward) of control siRNA-injected (D, F) and comm2 knockdown siRNA-injected (E, G, H) embryos at 53 hours of development. In control-injected nerve cords (D, F), which have a wild-type appearance, the anterior commissure is marked by a black arrow while a white arrow marks the posterior commissure. Knockdown of comm2 results in loss of commissural axons (E, G, H). Comparable results were obtained with two different siRNAs (comm2 siRNA-1 in E, G; comm2 siRNA-2 in H). Panels F and G show high magnification views of the nerve cords in D and E, respectively.