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Structural characterization of the mouse high growth deletion and discovery of a novel fusion transcript between suppressor of cytokine signaling-2 (Socs-2) and viral encoded semaphorin receptor (Plexin C1).

作者信息

Wong Marisa L, Islas-Trejo Alma, Medrano Juan F

机构信息

Department of Animal Science, University of California, One Shields Avenue, Davis, CA 95616-8521, USA.

出版信息

Gene. 2002 Oct 16;299(1-2):153-63. doi: 10.1016/s0378-1119(02)01052-1.

Abstract

The high growth (HG) mouse mutation is a 460 Kb deletion of chromosome 10 which causes a 30-50% increase in growth in the homozygous animal. We have shotgun sequenced six bacterial artificial chromosomes which span the length of the deletion to an average depth of 13.2x to generate a 649,868 bp sequence. Sequence analysis revealed the presence of three genes, suppressor of cytokine signaling-2 (Socs-2), caspase and RIP adaptor with death domain (Raidd/Cradd), and viral encoded semaphorin receptor (Plexin C1, viral encoded semaphorin receptor). The two deletion breakpoints lie in within the second introns of both Socs-2 and Plexin C1, resulting in the formation of a novel expressed fusion transcript between Socs-2 and Plexin C1 in HG mice. Expression of the fusion transcript, the presence of four splice variants of Raidd/Cradd and the exon structure of Socs-2 were illustrated using polymerase chain reaction. Genomic comparisons of the mouse and human sequence were used to verify the sequence assembly.

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