TRE-ATTAC (tetracycline-responsive-element-apoptosis through targeted activation of caspase-8) transgenic mice express human caspase 8 fused to serial FKBPv (Phe36Val mutant FKBP) dimerization domains driven by a tetracycline-responsive promoter element (TRE or tetO). A myristoylation site was included to provide membrane attachment for the caspase 8/FKBP fusion protein expression under the control of the TRE. When combined with doxycycline-inducible Tet-On reverse tetracycline-controlled transactivator (rtTA) protein and the injection of a dimerization agent that uniquely binds to the FKBP mutant protein, cell-specific widespread apoptosis is triggered. For example, when combined with mice carrying Lrat-rtTA (Stock No. <a href="https://www.jax.org/strain/041088" target="_blank">041088</a>), double-transgenic mice can be used to induce caspase-8-mediated apoptotic cell death that can be activated by the addition of a small-molecule dimerizer (AP20187) and doxycycline. Hemizygous mice are viable and fertile with no reported phenotype abnormalities. The donating investigator did not attempt to make a homozygous colony, and it is unknown if homozygotes are viable and fertile.

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TRE-ATTAC (tetracycline-responsive-element-apoptosis through targeted activation of caspase-8) mice enable doxycycline-inducible expression of a mutant FKBP fusion protein, which, upon dimerization, induces caspase-mediated apoptosis specifically in target cells/tissues upon injection of a construct-specific agent when combined with a Tet-On reverse tetracycline-controlled transactivator (rtTA) protein. This mouse is useful for targeted apoptosis in specific cells/tissues.