The Role of Genotype in the Formation of Leydig Cell Hormone Function during Postnatal Ontogeny in Diallele Crosses of Laboratory Mice

The Role of Genotype in the Formation of Leydig Cell Hormone Function during Postnatal Ontogeny... Production of testosterone by Leydig cells in the postnatal ontogeny during sexual maturation under in vitro stimulation by chorionic gonadotropin, dibutiryl-cAMP, and pregnenolon was studied in males of four inbred mouse lines (BALB/c, PT, CBA/Lac, and A/He) and their F1 reciprocal hybrids. Highly statistically significant association between the animal genotype and age was revealed for all parameters studied, which indicates the genotype-dependent formation of the Leydig cell hormone function during the postnatal ontogeny. The effect of genotype was characterized by two specific features. First, in each postnatal ontogeny stage examined correlative genetic variability of the cAMP- and substrate-dependent Leydig cell responsiveness was observed. Second, during postnatal ontogeny coordinated genetic variability underwent substantial ontogenetic changes. Definite pattern of genetic differences in the Leydig cell hormone activity was formed only at the late pubertal–early post-pubertal stage (60th day after birth). This process coincided with the completion of the Leydig cell morphological differentiation and the appearance of mature cells in the population. Thus, formation of the Leydig cell hormone function during postnatal ontogeny is under coordinated genetic control, which itself undergoes significant changes during sexual maturation. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Russian Journal of Genetics Springer Journals

The Role of Genotype in the Formation of Leydig Cell Hormone Function during Postnatal Ontogeny in Diallele Crosses of Laboratory Mice

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Publisher
Kluwer Academic Publishers-Plenum Publishers
Copyright
Copyright © 2002 by MAIK “Nauka/Interperiodica”
Subject
Biomedicine; Human Genetics
ISSN
1022-7954
eISSN
1608-3369
D.O.I.
10.1023/A:1014377926163
Publisher site
See Article on Publisher Site

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