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The axon guidance defect of the telencephalic commissures of the JSAP1-deficient brain was partially rescued by the transgenic expression of JIP1

Title
The axon guidance defect of the telencephalic commissures of the JSAP1-deficient brain was partially rescued by the transgenic expression of JIP1
Authors
Ha H.-Y.Cho I.-H.Lee K.-W.Song J.-Y.Kim K.-S.Yu Y.-M.Lee J.-K.Song J.-S.Yang S.-D.Shin H.-S.Han P.-L.
Ewha Authors
한평림
SCOPUS Author ID
한평림scopus
Issue Date
2005
Journal Title
Developmental Biology
ISSN
0012-1606JCR Link
Citation
Developmental Biology vol. 277, no. 1, pp. 184 - 199
Indexed
SCI; SCIE; SCOPUS WOS scopus
Document Type
Article
Abstract
The JNK interacting protein, JSAP1, has been identified as a scaffold protein for mitogen-activated protein kinase (MAPK) signaling pathways and as a linker protein for the cargo transport along the axons. To investigate the physiological function of JSAP1 in vivo, we generated mice lacking JSAP1. The JSAP1 null mutation produced various developmental deficits in the brain, including an axon guidance defect of the corpus callosum, in which phospho-FAK and phospho-JNK were distributed at reduced levels. The axon guidance defect of the corpus callosum in the jsap1 -/- brain was correlated with the misplacement of glial sling cells, which reverted to their normal position after the transgenic expression of JNK interacting protein 1(JIP1). The transgenic JIP1 partially rescued the axon guidance defect of the corpus callosum and the anterior commissure of the jsap1 -/- brain. The JSAP1 null mutation impaired the normal distribution of the Ca +2 regulating protein, calretinin, but not the synaptic vesicle marker, SNAP-25, along the axons of the thalamocortical tract. These results suggest that JSAP1 is required for the axon guidance of the telencephalic commissures and the distribution of cellular protein(s) along axons in vivo, and that the signaling network organized commonly by JIP1 and JSAP1 regulates the axon guidance in the developing brain. © 2004 Elsevier Inc. All rights reserved.
DOI
10.1016/j.ydbio.2004.09.019
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일반대학원 > 뇌·인지과학과 > Journal papers
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