The DNA-Damage-Inducible Transcript 4-Like protein encoded by the Ddit4l gene is involved in the mTOR signalling pathway and thus, autophagy.
In these transgenic mice the HA-DDiT4L transgene expression is regulated by the tetracycline-responsive regulatory element (tetO).
When crossed with a tTA, tetracycline transactivator (tTA; "Tet-off") strain, human influenza hemagglutinin tagged Ddit4l transgene expression can be regulated with the tetracycline analog, doxycycline, in the resulting double mutant mice. Mutant mice expressing the HA-DDiT4L transgene from birth exhibit mild ventricular remodeling and baseline systolic cardiac dysfunction. Homozygotes are viable and fertile. The Donating Investigator has not compared the phenotypes between hemizygous and homozygous animals. When crossed with a myocardial specific tTA, tetracycline transactivator (tTA; "Tet-off"), strain, with removal of doxycycline treatment the resulting double transgenic mice exhibit cardiac DDIT4L levels similar to that observed after TAC (transverse aortic constriction) induced hypertrophy and increased autophagy. Upon withdrawal of doxycycline, transgene expression is detected in heart, but not in lung, skeletal muscle, and liver.

These transgenic animals carry the HA tagged mouse DNA-damage-inducible transcript 4-like (Ddit4l) driven by a conditional mouse Myh6-tetO cardiac-specific promoter. When crossed with a tTA/rtTA strain, these mice may be useful in studies of cardiomyopathy.

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