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The Berlin Fat Mouse Inbred (BFMI) line is a model for juvenile obesity. Previous studies on crosses between BFMI and C57Bl/6N (B6N) have identified a recessive defect causing juvenile obesity on chromosome 3 ( jObes1 ).  Bbs7  was identified as the most likely candidate gene for the observed effect. Comparative sequence analysis showed a 1578 bp deletion in intron 8 of  Bbs7  in BFMI mice. A CTCF-element is located inside this deletion. To investigate the functional effect of this deletion, it was introduced into B6N mice using CRISPR/Cas9. Two mice containing the target deletion were obtained (B6N  Bbs 7 emI8∆1  and  Bbs7  emI8∆2 ) and were subsequently mated to BFMI and B6N to generate two families suitable for complementation. Inherited alleles were determined and body composition was measured by quantitative magnetic resonance. Evidence for a partial complementation (13.1–15.1%) of the  jObes1  allele by the CRISPR/Cas9 modified B6N  Bbs 7 emI8∆1  and  Bbs7  emI8∆2  alleles was found. Mice carrying the complementation alleles had a 23–27% higher fat-to-lean ratio compared to animals which have a B6N allele ( P  (Bbs7emI8∆1)  = 4.25 × 10 –7 ;  P  (Bbs7emI8∆2)  = 3.17 × 10 –5 ). Consistent with previous findings, the recessive effect of the BFMI allele was also seen for the B6N  Bbs 7 emI8∆1  and  Bbs7  emI8∆2  alleles. However, the effect size of the B6N  Bbs7   emI8 ∆1  and  Bbs7   emI8 ∆2  alleles was smaller than the BFMI allele, and thus showed only a partial complementation. Findings suggest additional variants near  Bbs7  in addition to or interacting with the deletion in intron 8.

A deletion containing a CTCF-element in intron 8 of the Bbs7 gene is partially responsible for juvenile obesity in the Berlin Fat Mouse