Development of the corticospinal tract in Semaphorin3A- and CD24-deficient mice.
Mutations in the gene encoding the neural recognition molecule L1 result in hypoplasia of the corticospinal tract and path finding errors of corticospinal axons at the pyramidal decussation. Candidate molecules that have been implicated in L1-dependent guidance of corticospinal axons from the ventral medullary pyramids to the contralateral dorsal columns of the cervical spinal cord include Semaphorin3A and CD24. In the present study, we anterogradely labeled corticospinal axons from the sensorimotor cortex of young postnatal Semaphorin3A- and CD24-deficient mice to elucidate potential functions of both proteins during formation of this long axon projection. Our results indicate that elongation, collateralization, fasciculation and path finding of corticospinal axons in mice proceed normally in the absence of Semaphorin3A or CD24.
Sibbe
M
M
Department of Ophthalmology, University Medical Centre Hamburg-Eppendorf, Martinistr. 52, 20246 Hamburg, Germany.
Taniguchi
M
M
Schachner
M
M
Bartsch
U
U
D000367:Age Factors; D000818:Animals; D000831:Animals, Newborn; D001369:Axons / Q000502:physiology; D051927:CD24 Antigen / Q000235:genetics*; D004622:Embryo, Mammalian; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D008817:Mice, Mutant Strains; D011712:Pyramidal Tracts / Q000166:cytology / Q000254:growth & development*; D040121:Semaphorin-3A / Q000172:deficiency*
D051927:CD24 Antigen; C488217:Sema3a protein, mouse; D040121:Semaphorin-3A