Targeted disruption of the Chop gene delays endoplasmic reticulum stress–mediated diabetes
J. Clin. Invest. Seiichi Oyadomari, et al. 109:525 doi:10.1172/JCI14550 [Go to this article.]

Figure 4
Characteristics of the double-mutant mice with Ins2 mutation and Chop disruption. (a) Genotyping of double-mutant mice. Representative genotyping of the Ins2 gene by RFLP; the Chop gene from nine mutant lines is shown by PCR. Ins2 exon 3 was amplified by PCR using genomic DNA. The Ins2^C96Y mutation in Akita mice disrupts an Fnu4HI site in exon 3 of Ins2. Digestion with Fnu4HI did not change the size of the PCR product from the mutated allele (280 bp), but it decreased that of the wild-type allele to 140 bp. Primers for wild-type and mutated Chop mice are described in Methods. The left lane shows 100-bp DNA ladder markers (top panel) and λDNA/Hind III + φ×174DNA/Hae III fragment markers (middle and bottom panels). (b–d) Phenotypic characterization of double-mutant mice at 8 weeks of age. (b) Body weight. (c) Morning blood glucose. (d) Pancreatic insulin content. Data are shown as mean ± SD. Significant differences among the genotype of the CHOP gene were evaluated by the Student t test: *P < 0.001 versus Chop^+/+. ^‡Ins2^C96Y/C96YChop^+/+ mice died within days of birth. Therefore, ^†data are shown as only one mouse and ^‡data are shown as means ± ranges (n = 2).