Eprs (glutamyl-prolyl-tRNA synthetase) encodes a multifunctional aminoacyl-tRNA synthetase that catalyzes the attachment of proline and glutamic acid to cognate tRNAs for protein synthesis. As such, Eprs is involved in the translational control of proline-rich profibrotic genes upregulated in cardiac fibrosis and heart failure. Eprs gKO mice were created using CRISPR/cas9 genome editing to insert tandem stop codons and a frame-shifting adenosine residue into exon 3 of the Eprs locus resulting in a null allele. Mice heterozygous for the mutation are viable and fertile. In the homozygous state, the mutation is embryonic lethal. Following isoproterenol (ISO) infusion, heterozygous mice developed less cardiac fibrosis then controls. Transverse aortic constriction (TAC) surgery resulted in a 40% reduction of cardiac fibrosis, partially restored cardiac function, and reduced cardiac hypertrophy in heterozygotes as compared to wild-type. Induction of myocardial infarction (MI) with artery ligation surgery also resulted in reduced cardiac fibrosis as compared to controls. These mice be useful in studies of the regulation of profibrotic genes during cardiac fibrosis.

Eprs gKO mice have premature stop codons inserted in exon 3 of the Eprs (glutamyl-prolyl-tRNA synthetase) locus. In the homozygous state, the mutation is embryonic lethal. Heterozygotes are resistant to isoproterenol, myocardial infarction (MI) and transverse aortic constriction (TAC)-induced cardiac fibrosis. These mice be useful in studies of the regulation of profibrotic genes during cardiac fibrosis.

This strain is hosted by NIH's MMRRC, which partners with JAX for the distribution of this and other strains. For additional information and to purchase, please visit the MMRRC site.