The "interferon-gamma reporter with endogenous polyA transcript" (GREAT) allele has an IRES-eYFP reporter cassette inserted between the translational stop codon and 3' UTR/polyA tail of the interferon gamma (Ifng) gene. Thus, the bicistronic IFNγ-IRES-eYFP mRNA is under control of the endogenous IFNγ promoter/enhancer regions with proper regulation defined by the endogenous 3' UTR and polyA tail. Expression of eYFP is observed by FACS/immunofluorescence microscopy in Ifng-expressing cell types; including innate immune responding cells (natural killer [NK] cells, natural killer T [NKT] cells) and cytotoxic T lymphocyte (CTL) effector cells of the adaptive immune response (CD4+ and CD8+T cells).
Of note, the donating investigator reports that these GREAT mice are a more useful tool than their IFNγ-IRES-YFP-BGHpolyA knockin (YETI) mice. Because the YETI allele has a bovine growth hormone polyA tail (rather than the endogenous IFN-γ polyA tail), homozygous YETI mice exhibit aberrant bicistronic IFNγ-IRES-YFP mRNA regulation that results in high IFN-γ blood levels and premature death. In contrast, homozygous GREAT mice are viable, fertile and normal in size, with proper transcript regulation defined by the endogenous IFN-γ 3' UTR/polyA tail.
