TY - JOUR
T1 - Cloning and developmental expression of the murine homolog of doublecortin
AU - Matsuo, Naoki
AU - Kawamoto, Shoko
AU - Matsubara, Kenichi
AU - Okubo, Kousaku
N1 - Funding Information:
We are grateful to Lucy Rowe (The Jackson Laboratory, USA) for analysis of linkage data, and valuable suggestions. This work was supported in part by a Grant-in-Aid for Creative Basic Research (Human Genome Program) from the Ministry of Education, Science and Culture, Japan.
PY - 1998/11/27
Y1 - 1998/11/27
N2 - While analyzing active genes in neonatal mouse hippocampus by quantitative 3'-cDNA collection, we identified a highly conserved murine homolog of doublecortin, the causative gene of X-linked lissencephaly (XLIS) and subcortical laminar heterotopia (SCLH) syndrome. The m-doublecortin cDNA contains nearly 8 kb 3' UTR homologous to hs-doublecortin. and it was mapped to the X chromosome. The expression of m-doublecortin is limited to the developing CNS, especially the cortical plate, supporting that XLIS/SCLH syndrome is associated with an arrest of neuronal migration in the cerebral cortex. The m-doublecortin mRNA was absent in the ventricular zone where neuronal precursors proliferate, and interestingly it was found in various brain structures that are not typically affected in patients with this syndrome.
AB - While analyzing active genes in neonatal mouse hippocampus by quantitative 3'-cDNA collection, we identified a highly conserved murine homolog of doublecortin, the causative gene of X-linked lissencephaly (XLIS) and subcortical laminar heterotopia (SCLH) syndrome. The m-doublecortin cDNA contains nearly 8 kb 3' UTR homologous to hs-doublecortin. and it was mapped to the X chromosome. The expression of m-doublecortin is limited to the developing CNS, especially the cortical plate, supporting that XLIS/SCLH syndrome is associated with an arrest of neuronal migration in the cerebral cortex. The m-doublecortin mRNA was absent in the ventricular zone where neuronal precursors proliferate, and interestingly it was found in various brain structures that are not typically affected in patients with this syndrome.
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U2 - 10.1006/bbrc.1998.9698
DO - 10.1006/bbrc.1998.9698
M3 - Article
C2 - 9837748
AN - SCOPUS:0032573459
SN - 0006-291X
VL - 252
SP - 571
EP - 576
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 3
ER -