Dopamine deficient cat-2, octopamine deficient tbh-1 and tyramine deficient tdc-1 mutants did not have significant defects.
To determine if DA regulates ejaculation, we looked at the behavior of tyrosine hydroxylase deficient cat-2 lf) cat-2 lfales.
Although the homologous mutation in the LPL-deficient cat results in marginal but significant increase of TGs in heterozygous males, but not in female animals, the HTG in our patient is rather severe.
Catalase-deficient (cat) cells showed a similar chronological life span (CLS) relative to the wild-type control upon growth on carbon and nitrogen sources that are not oxidized by peroxisomal enzymes.
In this study we analyzed the CLS of wild-type (WT) and catalase-deficient (cat) H. polymorpha cells upon cultivation on media containing different carbon and nitrogen sources that do or do not involve peroxisome function.
Murakami et al. showed that dopamine-deficient cat-2 mutants have a normal lifespan when measured in standard culture conditions [ 2].
It has been reported that isoflurane anesthesia or stress induced rhabdomyolosis, hyperkalemia and death in dystrophin-deficient cats [ 25].
Moreover, taurine depletion by taurine-deficient diet in cats causes various pathological conditions, including retinal degeneration, reproductive failure and dilated cardiomyopathy (Hayes et al. 1975; Pion et al. 1987; Sturman 1991).
There are a few naturally occurring animal models of DGC-associated muscular dystrophy (e.g. the dystrophin-deficient mdx mouse, dystrophic golden retriever dog, HFMD cat and the δ-sarcoglycan-deficient BIO 14.6 cardiomyopathic hamster) that share common genetic protein abnormalities similar to those of the human disease.
Experiments by Vinny Naidoo (University of Pretoria) have shown that Gyps and other vulture species have an unusual metabolism with respect to NSAIDs [ 16]; they are suggested to be CYP 2C9 deficient or diminished, as are cats, which are also highly sensitive to NSAIDs and so may provide a pharmacokinetic model for vultures.
Indeed, CAT-1-deficient mice die rapidly after birth (Perkins et al. 1997), and the spared prenatal development of CAT-1-deficient mice is thought to result from the high levels of CAT-3 expressed in embryonic tissues (Ito and Groudine 1997; Nicholson et al. 1998).
