Source data for Nature Communications publication entitled "Factors other than hTau overexpression that contribute to tauopathy-like phenotype in rTg4510 mice"

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Gamache-etal-Ncomms-2019

Source data for Nature Communications publication entitled "Factors other than hTau overexpression that contribute to tauopathy-like phenotype in rTg4510 mice"

Datacite.yml
Title Factors other than hTau overexpression that contribute to tauopathy-like phenotype in rTg4510 mice
Authors Gamache,Julia;N. Bud Grossman Center for Memory Research and Care, Department of Neurology, University of Minnesota, Minneapolis, MN 55414;0000-0002-3750-147X
Benzow,Kellie;Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, MN 55414
Forster,Colleen;Histology & Research Laboratory, Clinical and Translational Science Institute, University of Minnesota, Minneapolis, 55414
Kemper,Lisa;N. Bud Grossman Center for Memory Research and Care, Department of Neurology, University of Minnesota, Minneapolis, MN 55414
Hlynialuk,Chris;N. Bud Grossman Center for Memory Research and Care, Department of Neurology, University of Minnesota, Minneapolis, MN 55414
Furrow,Eva;Veterinary Clinical Sciences (College of Veterinary Medicine), University of Minnesota, Minneapolis, MN 55414
Ashe,Karen H.;N. Bud Grossman Center for Memory Research and Care, Department of Neurology, University of Minnesota, Minneapolis, MN 55414
Koob,Michael D.;Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, MN 55414
Description The tauopathy-like phenotype observed in the rTg4510 mouse line, in which human tauP301L expression specifically within the forebrain can be temporally controlled, has largely been attributed to high overexpression of mutant human tau in the forebrain region. Unexpectedly, we found that in a different mouse line with a targeted-insertion of the same transgene driven by the same tetracycline-TransActivator (tTA) allele, but with even higher overexpression of tauP301L than rTg4510, atrophy and tau histopathology are delayed, and a different behavioral profile is observed. This suggests that it is not overexpression of mutant human tau alone that contributes to the phenotype in rTg4510 mice. Furthermore we show that the tauopathy-like phenotype seen in rTg4510 requires a ~70-copy tau-transgene insertion in a 244kb deletion in Fgf14, a ~7-copy tTA- transgene insertion in a 508kb deletion that disrupts another five genes, in addition to high transgene overexpression. We propose that these additional effects need to be accounted for in any studies using rTg4510, and that Tg-INDEL mutations and their impacts on phenotype should be defined for all transgenic models used in biomedical research.
License Creative Commons CC0 1.0 Public Domain Dedication (https://creativecommons.org/publicdomain/zero/1.0/)
References
Funding
Keywords Neuroscience
Transgene
rTg4510
Tau
Fgf14
Resource Type Dataset