Plant, Animal & Microbe Genomes X Conference

January 12-16, 2002
Town & Country Convention Center
San Diego, CA

Poster: Genome Sequencing & ESTs
            

SEQUENCE ANALYSIS OF A 660 KB REGION ON MOUSE CHROMOSOME 10 ASSOCIATED WITH THE HIGH GROWTH PHENOTYPE.

¹ Department of Animal Science, University of California, One Shields Avenue, Davis, CA 95616, USA

² Zootechnical Department, Biotechnical Faculty, University of Ljubljana, SLOVENIA

The high growth (hg) mutation in mice is characterized by a 30-50% increase in growth in the homozygous state, and is due to a spontaneously occurring 460 Kb deletion of chromosome 10. To determine the gene or genes responsible for this phenotype, we have shotgun sequenced six BACs which span the length of the deletion to an average depth of 13.2x in order to generate a set of 12 contigs which have been ordered and oriented to create a single contiguous sequence of 658,895 bp. Sequence annotation by comparison to the NCBI non-redundant (nr) and EST databases revealed the presence of three genes, suppressor of cytokine signaling-2 (Socs-2), caspase and RIP adaptor with death domain (Raidd/Cradd), and Plexin C1 (Vespr). Northern blot analysis of Socs-2 and Raidd/Cradd revealed the absence of expression in hg/hg mice, verifying these two genes are contained within the deletion. It has been confirmed that the lack of Socs-2 gene product is the primary cause of the HG phenotype (Genomics 72:209-12, 2001). Vespr lies immediately adjacent to the deletion breakpoint (the start of the first exon is within 1 Kb) and is expressed in hg/hg mice. To determine the structure of the genes within the deletion, mRNA and clustered EST sequences of each gene were used in pair-wise comparisons against our genomic sequence. This resulted in the definition of exon/intron boundaries as well as revealed the presence of several splice variants of Raidd/Cradd.