Faculty Research 1990 - 1999

Chromosomal mapping of mouse genes expressed selectively within the central nervous system.

Document Type

Article

Publication Date

1994

Keywords

Brain: me, Central-Nervous-System: me, Chromosome-Mapping, Comparative-Study, Crosses-Genetic, Female, Gene-Expression-Regulation, Hybridization, Male, Mice: ge, me, Mice-Inbred-C57BL, Muridae: ge, Nerve-Tissue-Proteins: bi, ge, Organ-Specificity, Restriction-Fragment-Length-Polymorphisms, SUPPORT-U-S-GOVT-P-H-S

First Page

454

Last Page

461

JAX Source

Genomics 1994 Feb;19(3):454-61

Grant

NS22111/NS/NINDS, NS22347/NS/NINDS, GM32355/GM/NIGMS

Abstract

We have used RFLP analysis on DNA from a panel of interspecific (C57BL/6J x Mus spretus) F1 x M. spretus backcross offspring to assign the genes encoding 10 neuron-specific mRNAs and 2 loci corresponding to cyclophilin 2-related sequences to the mouse chromosomal map. The Pss1 locus encoding the forebrain-enriched protein kinase C substrate RC3, a component of dendritic spines, mapped to proximal Chr 9. The Camkl locus encoding the calmodulin-binding protein kinase-like vesicle protein 1G5 mapped to distal Chr 9. The Gng7 locus encoding the gamma 7 G-protein subunit, highly enriched in the striatum and presumptively coupled to dopamine receptors, mapped to mid-Chr 10. The Htr1f, Htr5a, Htr5b, and Htr7loci, encoding four serotonin receptors, mapped to Chr 16, 5, 1, and 19, respectively. The Peplb locus, encoding a CD26 ectopeptidase-like neuronal membrane protein activated by kainate and long-term potentiation, mapped to Chr 5. The D2Sut1e and Cpu3 loci, encoding neural proteins of unknown functions, mapped to Chrs 2 and 9, respectively. Two cyclophilin 2-related loci, Cphn2-r1 and Cphn2-r2, mapped to different regions of Chr 9. Comparison of these 12 newly mapped loci with the existing mouse map and known regions of syntenic homology with the human map, along with the known features and expression profiles of the products of these genes, suggests a few candidates for mouse mutations and human neurological and immunological deficits, including the Tourette syndrome and Bloom syndrome genes.

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