Deletion of SOCS7 leads to enhanced insulin action and enlarged islets of Langerhans
J. Clin. Invest. Alexander S. Banks, et al. 115:2462 doi:10.1172/JCI23853 [
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Figure 2Targeted disruption of the
Socs7 gene by homologous recombination. (
A) Schematic representation of mouse
Socs7 gene (top), targeting construct (middle), and targeted allele (bottom). Relevant restriction sites are indicated: Bg, BglII; H, HindIII; N, NotI; S, SalI; X, XbaI. The black boxes indicate exons. Neo
R refers to the positive selection marker. The genomic fragment used as a probe for Southern blot analysis and the expected fragments after BglII digestion are indicated. (
B) Southern blot analysis of BglII-digested genomic DNA from ES cell clones. The blot was hybridized with the indicated 3′ external probe. Lanes 1 and 2 show the wild-type allele from MEF and ES cells. Lanes 3–8 are from ES cells with correctly targeted alleles. (
C) PCR analysis of genomic DNA from the tails of wild-type, heterozygous (Het), and knockout littermates. (
D) Northern blot analysis of liver, skeletal muscle, and testis from wild-type, heterozygous, and knockout mice, showing the absence of
Socs7 full-length transcript expression. (
E) Growth retardation and hydrocephalus in
Socs7 –/ – C57BL/6 mice. At 20 days of age, affected knockout mice exhibited a 40% decrease in weight when compared with heterozygote littermates on the C57BL/6 background (upper panel). Severe hydrocephalus is also present in a 4-week-old
Socs7 –/ – mouse (lower panels). Hydrocephalus was not apparent in the mixed-background mice used in this study (image not shown).
