International Mammalian Genome Society

The 13th International Mouse Genome Conference
October 31-November 3, 1999

Table of Contents * Structure * Bioinformatics * Sequence * Mapping * New Tools * Gene Discovery * Developmental * Mutagenesis * Functional Genomics

E24 A Four-Locus Least Squares Linear Genetic Model of Testosterone Production by Leydig Cell in Mice

Osadchuk, A. V., Svechnikov, K. V., and Ahmerova, L G. Institute Cytology and Genetics of Siberian Branch of Russian Academy of Sciences, Novosibirsk, 630090, Russia

In the present study, we investigated genetic control of testicular steroidogenesis with an emphasis on the analysis of inheritance variation due to genes with mild action, not resulting in disruption of the reproductive function and development of sterility, and, hence, widespread in human and mammalian populations. Previously, we disclosed the coordinated interstrain variations in cAMP- and substrate-dependent testosterone production by Leydig cells in six inbred mouse strains contrasting in plasma testosterone, reproductive success and social dominance. Subsequently, we demonstrated the coordinated interstrain variability in microsomal steroidogenic enzyme activities that caused this hereditary polymorphism. To detect the genetic architecture of testicular steroidogenesis, a diallel study of hCG-, cAMP-, pregnenolone-, progesterone-, and androstenedione-stimulated testosterone productions by Leydig cells in mature males of six inbred mouse strains (BALB/c, A/He, CBA/Lac, DD, YT and PT) and their F1 reciprocal hybrids was performed. There were highly significant genotype-dependent correlations between the above traits. Furthermore, the inheritance patterns of cAMP- and substrate-dependent testosterone production were very similar. Phenotypic variations in the testosterone production were significantly determined by the following components: interstrain effects, general and specific combining ability effects, residual reciprocal effects and mean directional dominance. Thus, the revealed genotype-dependent variations in cAMP- and substrate-dependent testosterone production by Leydig cells were simultaneously under coordinated and polygenic genetic control. Based on the discriminant and multiple regression analysis, we developed a four-locus genetic model accounting for more than 90% of the genotype-dependent variation. One or two of these loci were linked to the sex chromosomes, the other three or two to the autosomes. Three of these loci manifested epistatic digenic interactions and the fourth autosomal locus had only additive and dominance effects. In conclusion, the existence of a four-locus genetic system determining the coordinated hereditary variability of Leydig cell hormonal activity was established for the first time. The developed genetic model is a good tool for the molecular-genetic analysis of testicular steroidogenesis. (This work was supported by the grant RFFR N 98-04-49452.)


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