C57BL/6J male mice bearing Mfn1 (Mfn1tm2Dcc; JAX stock no. 026401) and Mfn2 (B6.129(Cg)-Mfn2tm3Dcc/J; JAX stock no. 026525; The Jackson Laboratory, Bar Harbor, ME) alleles (20 (link)) with loxP sites flanking exons 4 and 6 were purchased from The Jackson Laboratory and crossed to C57BL/6J transgenic animals carrying an inducible Cre recombinase under Pdx1 promoter control (Pdx1-CreERT2) (21 (link)). Mice bearing floxed Mfn alleles but lacking Cre recombinase were used as littermate controls in this study. Mice were genotyped following protocols described by The Jackson Laboratory for each of these strains (see Supplementary Table 1 ). Recombination was achieved by daily tamoxifen (10 mg/mouse diluted in corn oil; Sigma-Aldrich, Dorset, U.K.) i.p. injections for 5 days at 7–8 weeks of age in both control and β-cell selective Mfn1/Mfn2 deletion knockout (dKO) (βMfn1/2 dKO) groups.
Animals with floxed Clec16a alleles were bred to mice carrying the Pdx1-Cre transgene (Clec16aΔpanc), as previously described (22 (link)). Pdx1-Cre alone mice were used as littermate controls. Pdx1CreER mice were generated as previously described (21 (link)).
Animals with floxed Clec16a alleles were bred to mice carrying the Pdx1-Cre transgene (Clec16aΔpanc), as previously described (22 (link)). Pdx1-Cre alone mice were used as littermate controls. Pdx1CreER mice were generated as previously described (21 (link)).
