LIS1: Cellular Function of a Disease-causing Gene

Overview

Journal Trends Cell Biol

Specialty Cell Biology

Date 2001 Apr 18

PMID 11306294

Citations 28

Authors

R B Vallee

C Tai

N E Faulkner

Affiliations

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Abstract

Brain development is severely defective in children with lissencephaly. The highly organized distribution of neurons within the cerebral cortex is disrupted, a condition that might arise from improper migration of neuronal progenitors to their cortical destinations. Type I lissencephaly results from mutations in the LIS1 gene, which has been implicated in the cytoplasmic dynein and platelet-activating factor pathways. Recent studies have identified roles for the product of LIS1 in nuclear migration, mitotic spindle orientation and chromosome alignment, where it appears to act in concert with cytoplasmic dynein. A unifying hypothesis for the subcellular function of LIS1 is presented.

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