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Lissencephaly gene (LIS1) expression in the CNS suggests a role in neuronal migration

O Reiner, U Albrecht, M Gordon, KA Chianese, C Wong, O Gal-Gerber, T Sapir, LD Siracusa, AM Buchberg and CT Caskey
Journal of Neuroscience 1 May 1995, 15 (5) 3730-3738; DOI: https://doi.org/10.1523/JNEUROSCI.15-05-03730.1995
O Reiner
Department of Molecular Genetics and Virology, Weizmann Institute of Science, Rehovot, Israel.
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U Albrecht
Department of Molecular Genetics and Virology, Weizmann Institute of Science, Rehovot, Israel.
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M Gordon
Department of Molecular Genetics and Virology, Weizmann Institute of Science, Rehovot, Israel.
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KA Chianese
Department of Molecular Genetics and Virology, Weizmann Institute of Science, Rehovot, Israel.
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C Wong
Department of Molecular Genetics and Virology, Weizmann Institute of Science, Rehovot, Israel.
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O Gal-Gerber
Department of Molecular Genetics and Virology, Weizmann Institute of Science, Rehovot, Israel.
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T Sapir
Department of Molecular Genetics and Virology, Weizmann Institute of Science, Rehovot, Israel.
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LD Siracusa
Department of Molecular Genetics and Virology, Weizmann Institute of Science, Rehovot, Israel.
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AM Buchberg
Department of Molecular Genetics and Virology, Weizmann Institute of Science, Rehovot, Israel.
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CT Caskey
Department of Molecular Genetics and Virology, Weizmann Institute of Science, Rehovot, Israel.
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Abstract

Miller-Dieker lissencephaly syndrome (MDS) is a human developmental brain malformation caused by neuronal migration defects resulting in abnormal layering of the cerebral cortex. LIS1, the gene defective in MDS, encodes a subunit of brain platelet-activating factor (PAF) acetylhydrolase which inactivates PAF, a neuroregulatory molecule. We have isolated murine cDNAs homologous to human LIS1 and mapped these to three different chromosomal loci (Lis1, Lis3, Lis4). The predicted sequences of murine Lis1 protein and its human homolog LIS1 are virtually identical. In the developing mouse and human, Lis1 and LIS1 genes were strongly expressed in the cortical plate. In the adult mouse Lis1 transcripts were abundant in cortex and hippocampus. The direct correlation between cortical defects in MDS patients and Lis1 expression in the murine cortex suggest that the mouse is a model system suitable to study the mechanistic basis of this intriguing genetic disease.

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The Journal of Neuroscience: 15 (5)
Journal of Neuroscience
Vol. 15, Issue 5
1 May 1995
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Lissencephaly gene (LIS1) expression in the CNS suggests a role in neuronal migration
O Reiner, U Albrecht, M Gordon, KA Chianese, C Wong, O Gal-Gerber, T Sapir, LD Siracusa, AM Buchberg, CT Caskey
Journal of Neuroscience 1 May 1995, 15 (5) 3730-3738; DOI: 10.1523/JNEUROSCI.15-05-03730.1995

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Lissencephaly gene (LIS1) expression in the CNS suggests a role in neuronal migration
O Reiner, U Albrecht, M Gordon, KA Chianese, C Wong, O Gal-Gerber, T Sapir, LD Siracusa, AM Buchberg, CT Caskey
Journal of Neuroscience 1 May 1995, 15 (5) 3730-3738; DOI: 10.1523/JNEUROSCI.15-05-03730.1995
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