The mice have a loxp-flanked transcriptional blocking (loxTB) sequence that prevents normal endogenous gene transcription and translation from the endogenous locus. As such, homozygous mice are devoid of functional mRNA in all tested regions of the brain. Homozygous mice exhibit obesity, accompanied by hyperphagia, increased snout-anus length and hyperinsulinemia. In 2018, The Jackson Laboratory colony, on the mixed B6;129S4 background and maintained on standard chow diet, shows that homozygous mice are significantly heavier than sex-matched wildtype controls by approximately 6-8 weeks of age (more obvious for female homozygotes at a younger age), and obesity (30g) is apparent at approximate 7 weeks of age for homozygous males and approximately 10 weeks of age for homozygous females.
The function of this disrupted allele can be restored by the enzymatic activity of Cre-recombinase. These mutant mice may be useful in studies of neurobiology, obesity, diabetes, hunger/appetite, and fat and energy metabolism.
When bred to a strain expressing Cre recombinase in the hypothalamus see Stock No. 006395 for example), this mutant mouse strain exhibits as intermediate phenotype in comparison to homozygous null mice.
When crossed to STOCK Slc32a1tm2(cre)Lowl/J (see Stock No. 016962) Cre recombinase expression in inhibitory GABAergic neuron cell bodies results in offspring that exhibit obesity.
When crossed to B6;129S-Oxttm1.1(cre)Dolsn/J (see Stock No. 024234) Cre recombinase expression in oxytocin-expressing cells results in offspring that exhibit obesity.
