MAP1B is required for Netrin 1 signaling in neuronal migration and axonal guidance

被引:106
作者
Del Río, JA
González-Billault, C
Ureña, JM
Jiménez, EM
Barallobre, MJ
Pascual, M
Pujadas, L
Simó, S
La Torre, A
Wandosell, F
Avila, J [1 ]
Soriano, E
机构
[1] Univ Barcelona, Barcelona Sci Pk & Dept Cell Biol, Inst Recerca Biomed Barcelona, Dev Neurobiol & Regenerat Unit, Barcelona 08028, Spain
[2] Univ Autonoma Madrid, Consejo Super Invest Cientificas, Ctr Biol Mol, Madrid 28049, Spain
关键词
D O I
10.1016/j.cub.2004.04.046
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Background: The signaling cascades governing neuronal migration and axonal guidance link extracellular signals to cytoskeletal components. MAP1B is a neuronspecific microtubule-associated protein implicated in the crosstalk between microtubules and actin filaments. Results: Here we show that Netrin 1 regulates, both in vivo and in vitro, mode I MAP1B phosphorylation, which controls MAP1B activity, in a signaling pathway that depends essentially on the kinases GSK3 and CDK5. We also show that map1B-deficient neurons from the lower rhombic lip and other brain regions have reduced chemoattractive responses to Netrin 1 in vitro. Furthermore, map1B mutant mice have severe abnormalities, similar to those described in netrin 1-deficient mice, in axonal tracts and in the pontine nuclei. Conclusions: These data indicate that MAP1B phosphorylation is controlled by Netrin 1 and that the lack of MAP1B impairs Netrin 1-mediated chemoattraction in vitro and in vivo. Thus, MAP1B may be a downstream effector in the Netrin 1-signaling pathway.
引用
收藏
页码:840 / 850
页数:11
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