Figure 8

Corticospinal tract (CST) projections in Sema6A and Plxn mutants. (a-j) Anti-L1-immunohistochemistry on P10 Sema6A^+/- (a, f), Sema6A^-/- (b, g), PlxnA2^-/- (c, h), PlxnA4^-/- (d, i), and PlxnA2^-/-;PlxnA4^-/- (e, j) mice. Anti-L1 staining in Sema6A^+/- mice highlights corticospinal tract (CST) axons turning ventrally over the pontine nuclei (a) and decussating at the caudal medulla (f). At the MHB of Sema6A^-/- mice (b), the number of CST axons is severely (left side) or moderately (right side) reduced. Only a few misguided axons can be found, indicating that most have already died between P4 and P10. At the decussation level (g), in some cases virtually no axons are left (left side). If CST axons are visible, they form a ventrolateral projection (arrowhead; right side), decussate properly (not shown; Figure 1), or split into two bundles to do both (not shown; Figure 1). PlxnA2^-/- mice show no apparent guidance defects or reduction in size of the CST (c, h). In PlxnA4^-/- mice, the size of the CST appears normal from the MHB (d), where no misguided axons can be found, up to the level of the caudal medulla. Here, the CST splits into two bundles that either form a ventral projection (white arrowhead in (i)) or join the contralateral dorsal funiculus (not shown). The phenotype in PlxnA2;PlxnA4 double mutants is indistinguishable from that in PlxnA4^-/- single mutants, with no apparent defect at the MHB (e) and an identical phenotype in the caudal medulla (j); white arrowheads indicate ventrolaterally projecting CST axons. Scale bar: 200 μm.