Close homolog of L1 and neuropilin 1 mediate guidance of thalamocortical axons at the ventral telencephalon.
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Close homolog of L1 and neuropilin 1 mediate guidance of thalamocortical axons at the ventral telencephalon. / Wright, Amanda G; Demyanenko, Galina P; Powell, Ashton; Schachner, Melitta; Enriquez-Barreto, Lilian; Tran, Tracy S; Polleux, Franck; Maness, Patricia F.
In: J NEUROSCI, Vol. 27, No. 50, 50, 2007, p. 13667-13679.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Close homolog of L1 and neuropilin 1 mediate guidance of thalamocortical axons at the ventral telencephalon.
AU - Wright, Amanda G
AU - Demyanenko, Galina P
AU - Powell, Ashton
AU - Schachner, Melitta
AU - Enriquez-Barreto, Lilian
AU - Tran, Tracy S
AU - Polleux, Franck
AU - Maness, Patricia F
PY - 2007
Y1 - 2007
N2 - We report a cooperation between the neural adhesion molecule close homolog of L1 (CHL1) and the semaphorin 3A (Sema3A) receptor, neuropilin 1 (Npn1), important for establishment of area-specific thalamocortical projections. CHL1 deletion in mice selectively disrupted the projection of somatosensory thalamic axons from the ventrobasal (VB) nuclei, causing them to shift caudally and target the visual cortex. At the ventral telencephalon, an intermediate target with graded Sema3A expression, VB axons were caudally shifted in CHL1- embryos and in Npn1(Sema-/-) mutants, in which axons are nonresponsive to Sema3A. CHL1 colocalized with Npn1 on thalamic axons, and associated with Npn1 through a sequence in the CHL1 Ig1 domain that was required for Sema3A-induced growth cone collapse. These results identify a novel function for CHL1 in thalamic axon responsiveness to ventral telencephalic cues, and demonstrate a role for CHL1 and Npn1 in establishment of proper targeting of specific thalamocortical projections.
AB - We report a cooperation between the neural adhesion molecule close homolog of L1 (CHL1) and the semaphorin 3A (Sema3A) receptor, neuropilin 1 (Npn1), important for establishment of area-specific thalamocortical projections. CHL1 deletion in mice selectively disrupted the projection of somatosensory thalamic axons from the ventrobasal (VB) nuclei, causing them to shift caudally and target the visual cortex. At the ventral telencephalon, an intermediate target with graded Sema3A expression, VB axons were caudally shifted in CHL1- embryos and in Npn1(Sema-/-) mutants, in which axons are nonresponsive to Sema3A. CHL1 colocalized with Npn1 on thalamic axons, and associated with Npn1 through a sequence in the CHL1 Ig1 domain that was required for Sema3A-induced growth cone collapse. These results identify a novel function for CHL1 in thalamic axon responsiveness to ventral telencephalic cues, and demonstrate a role for CHL1 and Npn1 in establishment of proper targeting of specific thalamocortical projections.
M3 - SCORING: Zeitschriftenaufsatz
VL - 27
SP - 13667
EP - 13679
JO - J NEUROSCI
JF - J NEUROSCI
SN - 0270-6474
IS - 50
M1 - 50
ER -