a focused and efficient genetic screening strategy in the mouse identification of mutations that disrupt cortical development鼠标的集中、高效的基因筛查策略识别突变破坏皮质的发展.pdfVIP

a focused and efficient genetic screening strategy in the mouse identification of mutations that disrupt cortical development鼠标的集中、高效的基因筛查策略识别突变破坏皮质的发展.pdf

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a focused and efficient genetic screening strategy in the mouse identification of mutations that disrupt cortical development鼠标的集中、高效的基因筛查策略识别突变破坏皮质的发展

Open access, freely available online PLoS BIOLOGY A Focused and Efficient Genetic Screening Strategy in the Mouse: Identification of Mutations That Disrupt Cortical Development 1[ 1[ 1 2 3 1* Konstantinos Zarbalis , Scott R. May , Yiguo Shen , Marc Ekker , John L. R. Rubenstein , Andrew S. Peterson 1 Department of Neurology and the Ernest Gallo Clinic and Research Center, University of California at San Francisco, Emeryville, California, United States of America, 2 Loeb Medical Research Institute, University of Ottawa, Ottawa, Ontario, Canada, 3 Nina Ireland Laboratory of Developmental Neurobiology, Department of Psychiatry, Langley Porter Psychiatric Institute, University of California at San Francisco, San Francisco, California, United States of America Although the mechanisms that regulate development of the cerebral cortex have begun to emerge, in large part through the analysis of mutant mice (Boncinelli et al. 2000; Molnar and Hannan 2000; Walsh and Goffinet 2000), many questions remain unanswered. To provide resources for further dissecting cortical development, we have carried out a focused screen for recessive mutations that disrupt cortical development. One aim of the screen was to identify mutants that disrupt the tangential migration of interneurons into the cortex. At the same time, we also screened for mutations that altered the growth or morphology of the cerebral cortex. We report here the identification of thirteen mutants with defects in aspects of cortical development ranging from the establishment of epithelial polarity to the invasion of thalamocortical axons. Among the collection are three novel alleles of genes for which mutant alleles had already

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