Fig. 3. Knockdown of Nrp1a results in abnormal CaP cell positioning even after
axon formation. Position of CaP cell bodies after axonogenesis was
examined using isl2 expression (purple) and mAb Sv2 (brown).
(A) Side view of a control embryo at the 28-somite stage. (B) A
Nrp1a-knockdown embryo at the 29-somite stage with an irregular CaP pattern.
(C,D) Horizontal sections of control and Nrp1a-knockdown
embryos. CaPs are indicated by stars. (E; left) Severe dislocation was
defined as the center of the CaP cell bodies being located in either the
anterior or the posterior quarter of the overlying somite (indicated by `Mar'
in the schema). (Right) Dislocation of CaP was significantly increased in
Nrp1a-knockdown embryos, as determined by Fisher's exact test of independence
(star, P<0.05).Nc, notochord. (F) Abnormal exit points of
CaP axons by two separate CaPs in Nrp1a-knockdown embryos. CaP axons were
labeled with mAb Sv2. (G) The positions of CaPs (stars) relative to MiP
and RoP (diamonds, labeled by isl1) were unaffected by Nrp1a
knockdown. (H) Different lengths of two axons from separate CaPs
correspond to those of a CaP and a VaP. One axon extended onto the ventral
myotome (*), whereas the other axon did not extend beyond the
horizontal myoseptum (**). Arrowhead shows the level of the
horizontal myoseptum. MiP axons extended normally along the dorsal pathway
(arrows). The numbers in A, B and F-H denote the somitic segment order. The
blue lines indicate segment borders. Scale bar: 50 µm.