Blocking Site-Specific Cleavage of Human Tau Delays Progression of Disease-Related Phenotypes in Genetically Matched Tau-Transgenic Mice Modeling Frontotemporal Dementia

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Figure 1.
Figure 1.

Engineering MAPT transgenes in responder mouse lines: A schematic illustration. Col1A1, collagen; Type I, α1 gene; 3′-UTR, the three prime untranslated region; G418R, an open reading frame encoding aminoglycoside phosphotransferase from the Tn5 transposon that confers resistance to geneticin; FRT, flippase (FLP) recognition target; HygroR, an open reading frame encoding aminoglycoside phosphotransferase from E. coli that confers resistance to hygromycin; Pgk promoter, the mouse phosphoglycerate kinase 1 promoter; ATG, the start codon; Prnp/MAPT, DNA sequence encoding the 0N4R isoform of human tau inserted in the mouse prion protein gene encoding partial introns 1 and 2 plus exons 2-3; SV40 poly(A), simian virus 40 polyadenylation tail; CAG promoter, a synthetic promoter engineered from the cytomegalovirus early enhancer element, the chicken β-actin promoter, and the splice acceptor of the rabbit β-globin gene; FLPe, an open reading frame encoding a fusion between simian virus 40 nuclear localization signal and the S. cerevisiae site-specific recombinase FLP.

  1. The Journal of Neuroscience vol. 42 no. 23 4737-4754
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