Expression of MYC in these transgenic mice is regulated by a tetracycline operator (tetO). MYC is a transcription factor involved in cellular proliferation and differentiation, and is often upregulated in tumors, leukemias and lymphomas. Hemizygous mice are viable and fertile, homozygotes do not survive. When mated to a mutant strain expressing tetracycline-controlled transactivator protein (tTA), expression of MYC protein may be regulated with tetracycline or its analog doxycycline (dox) in the double mutant offspring.
When bred to B6.Cg-Tg(Cebpb-tTA)5Bjd/J mice (as Stock No. 003563) expressing tTA in liver, withdrawal of dox from double transgenic mice develop invasive metastatic liver tumors, and all mice die within 2 weeks onset. When doxycycline treatment is re-administered, rapid and sustained tumor regression is evident.
When bred to B6.Cg-Tg(Pax8-rtTA2S*M2)1Koes/J (see Stock No. 007176) expressing rtTA in renal tubular epithelial cells, induction of doxycycline causes polycystic kidneys, kidney failure and renal adenomas.
Of note: in B6.FVB-Tg(tetO-MYC)36aBop/DwfJ (Stock No. 034532) the tet-o-MYC transgene inserted on the Y chromosome and is transmitted only through males.
