The molecular basis of the obese mutation in ob2JMice
BC Moon, JM Friedman - Genomics, 1997 - Elsevier
BC Moon, JM Friedman
Genomics, 1997•ElsevierThe recessive ob2Jmutation in mice results in an obese phenotype that is identical to that of
the original ob allele. Initial studies indicated that ob2Jmice fail to synthesize ob RNA in
adipose tissue. Here we report the genomic organization of the mouse obese gene and
establish the molecular genetic basis of the ob2Jmutation. The ob2Jmutation is the result of
the insertion of a retroviral-like tranposon in the first intron of the ob gene. The insertion is a
member of the ETn family of transposons and contains several splice acceptor and …
the original ob allele. Initial studies indicated that ob2Jmice fail to synthesize ob RNA in
adipose tissue. Here we report the genomic organization of the mouse obese gene and
establish the molecular genetic basis of the ob2Jmutation. The ob2Jmutation is the result of
the insertion of a retroviral-like tranposon in the first intron of the ob gene. The insertion is a
member of the ETn family of transposons and contains several splice acceptor and …
The recessive ob2Jmutation in mice results in an obese phenotype that is identical to that of the original ob allele. Initial studies indicated that ob2Jmice fail to synthesize ob RNA in adipose tissue. Here we report the genomic organization of the mouse obese gene and establish the molecular genetic basis of the ob2Jmutation. The ob2Jmutation is the result of the insertion of a retroviral-like tranposon in the first intron of the ob gene. The insertion is a member of the ETn family of transposons and contains several splice acceptor and polyadenylation sites. This leads to the production of chimeric RNAs in which the ob first exon is spliced to sequences in the ETn insertion. As a consequence mature ob RNA is not synthesized, and leptin, the encoded protein, is not produced.
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