| First Author | Hasegawa Y | Year | 2016 |
| Journal | Exp Anim | Volume | 65 |
| Issue | 3 | Pages | 319-27 |
| PubMed ID | 27053096 | Mgi Jnum | J:240225 |
| Mgi Id | MGI:5882671 | Doi | 10.1538/expanim.16-0016 |
| Citation | Hasegawa Y, et al. (2016) Generation of CRISPR/Cas9-mediated bicistronic knock-in ins1-cre driver mice. Exp Anim 65(3):319-27 |
| abstractText | In the present study, we generated novel cre driver mice for gene manipulation in pancreatic beta cells. Using the CRISPR/Cas9 system, stop codon sequences of Ins1 were targeted for insertion of cre, including 2A sequences. A founder of C57BL/6J-Ins1(em1 (cre) Utr) strain was produced from an oocyte injected with pX330 containing the sequences encoding gRNA and Cas9 and a DNA donor plasmid carrying 2A-cre. (R26GRR x C57BL/6J-Ins1(em1 (cre) Utr)) F1 mice were histologically characterized for cre-loxP recombination in the embryonic and adult stages; cre-loxP recombination was observed in all pancreatic islets examined in which almost all insulin-positive cells showed tdsRed fluorescence, suggesting beta cell-specific recombination. Furthermore, there were no significant differences in results of glucose tolerance test among genotypes (homo/hetero/wild). Taken together, these observations indicated that C57BL/6J-Ins1(em1 (cre) Utr) is useful for studies of glucose metabolism and the strategy of bicistronic cre knock-in using the CRISPR/Cas9 system could be useful for production of cre driver mice. |
