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Volume 17, Number 23, Issue of December 1, 1997 pp. 9204-9211

Birthdate and Cell Marker Analysis of Scrambler: A Novel Mutation Affecting Cortical Development with a Reeler-Like Phenotype

Received May 13, 1997; revised Sept. 16, 1997; accepted Sept. 18, 1997.

Jorge L. González¹, Christopher J. Russo¹, Dan Goldowitz², Hope O. Sweet³, Muriel T. Davisson³, and Christopher A. Walsh¹

¹ Division of Neurogenetics, Department of Neurology, Beth Israel Deaconess Medical Center, and Program in Neuroscience, Harvard Medical School, Boston, Massachusetts 02115, ² Department of Anatomy and Neurobiology, University of Tennessee, Memphis, Tennessee 38163, and ³ The Jackson Laboratory, Bar Harbor, Maine 04609

The reeler mutation in mice produces an especially well characterized disorder, with systematically abnormal migration of cerebral cortical neurons. The reeler gene encodes a large protein, termed Reelin, that in the cortex is synthesized and secreted exclusively in the Cajal-Retzius neurons of the cortical marginal zone (). In reeler mutant mice, loss of Reelin protein is associated with a systematic loss of the normal, "inside-out" sequence of neurogenesis in the cortex: neurons are formed in the normal sequence but become localized in the cortex in a somewhat inverted, although relatively disorganized "outside-in" pattern. Here we show that the scrambler mutant mouse exhibits a loss of lamination in the cortex and hippocampus that is indistinguishable from that seen in the reeler mouse. We use BrdU birthdating studies to show that scrambler cortex shows a somewhat inverted "outside-in" sequence of birthdates for cortical neurons that is similar to that previously described in reeler cortex. Finally, we perform staining with the CR-50 monoclonal antibody (), which recognizes the Reelin protein (). We show that Reelin immunoreactivity is present in the scrambler cortex in a normal pattern, suggesting that Reelin is synthesized and released normally. Our data suggest that scrambler is a mutation in the same gene pathway as the reeler gene (Reln^rl) and is most likely downstream of Reln^rl.

Key words: cortex; neuronal migration; genetics; reeler; migration; scrambler; development; mdab1; Reelin

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