Breeding of Cav2.3 deficient mice reveals Mendelian inheritance in contrast to complex inheritance in Cav3.2 null mutant breeding

High voltage-activated Ca(v)2.3 R-type Ca2+ channels and low voltage-activated Ca(v)3.2 T-type Ca2+ channels were reported to be involved in numerous physiological and pathophysiological processes. Many of these findings are based on studies in Ca(v)2.3 and Ca(v)3.2 deficient mice. Recently, it has been proposed that inbreeding of Ca(v)2.3 and Ca(v)3.2 deficient mice exhibits significant deviation from Mendelian inheritance and might be an indication for potential prenatal lethality in these lines. In our study, we analyzed 926 offspring from Ca(v)3.2 breedings and 1142 offspring from Ca(v)2.3 breedings. Our results demonstrate that breeding of Ca(v)2.3 deficient mice shows typical Mendelian inheritance and that there is no indication of prenatal lethality. In contrast, Ca(v)3.2 breeding exhibits a complex inheritance pattern. It might be speculated that the differences in inheritance, particularly for Ca(v)2.3 breeding, are related to other factors, such as genetic specificities of the mutant lines, compensatory mechanisms and altered sperm activity.

Automated summary

The breeding of Ca(v)2.3 deficient mice follows typical Mendelian inheritance with no indication of prenatal lethality, while the breeding of Ca(v)3.2 deficient mice exhibits a complex inheritance pattern. Various factors such as genetic specificities, compensatory mechanisms, and altered sperm activity may contribute to the differences in inheritance patterns observed.