The overexpression of PXT1 in mouse testis leads to germ cell apoptosis and male infertility. The PXT1 protein contains a functional BH3-motif. PXT1 protein interacts with BAT3, and BAT3 is able to protect cells from PXT1-induced apoptosis.
In all living organisms trace element metabolism and transport are closely regulated at the genetic level. Copper is one of the essential microelements required for normal growth and development. The main organ in mammals involved in copper metabolism is the liver. It is known that copper metabolism in the liver is controlled by ATP7B, a P-type ATP-ase encoded by the Atp7b gene. However, little is known about the expression and function of the second important P-type ATP-ase, ATP7A encoded by the Atp7a gene. In this study we investigated the expression of the Atp7a gene in the liver during postnatal development in mice. We analyzed expression of Atp7a gene in the livers from neonatal (P.05), young (P14) and adult (P240) mice using RT-PCR and real-time PCR method. We found a transcript of the Atp7a gene in the liver of all investigated animals. Moreover, we found that the expression of the Atp7a gene in the liver in mice is age-dependent and decreases during postnatal development. Interestingly, the Atp7a expression in adult mice is very low in comparison with neonatal and young animals. Western blot analysis revealed that Atp7a is expressed not only at mRNA level but also at the protein level in the liver of all investigated animals. The expression of Atp7a gene and ATP7A protein was also confirmed in primary hepatocytes from adult mouse. Demonstration of the hepatic Atp7a gene expression may shed light on new aspects of copper metabolism in the liver in mammals.
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