title: Steroidogenesis expression depends on negative control(s): analysis in Leydig X adrenal intraspecific cell hybrids.
abstract: Hybrids constructed by fusing mouse Leydig cells with mouse adrenal Y1 cells were able to randomly express all the parental specific traits but for the response to gonadotropin (hCG) and corticotropin (ACTH): three of them, YDYL 14, 17 and 19, metabolized both progesterone and dehydroepiandrosterone into testosterone accounting for 17 alpha-hydroxylase, 17-20-lyase, 17-ketoreductase and 3 beta-hydroxysteroid dehydrogenase activities. Under basal conditions, 17 alpha-hydroxylase and 17-20-lyase activities were high in the three clones as compared to parental Leydig cells, and were no longer stimulated by cAMP in YDYL 17 and 19. The hybrids responded to various hormones such as prostaglandin E2 (PGE2), vasoactive intestinal peptide (VIP) and prolactin (PRL) which are not directly implicated in the expression of steroidogenesis; they generally retained the Y1 morphological response to 8-bromo cAMP. On extended culture, reexpression of ACTH sensitivity occurred in one clone, YDYL 9. This reexpression was correlated with a Robertsonian translocation between mouse chromosomes 2 and 11, while extinction required the presence of an intact mouse chromosome 11.
authors.affiliation: INSERM/CNRS, Hôpital Debrousse, Lyon, France.
authors.forename: A
authors.initials: A
authors.lastname: Lefèvre
authors.forename: M
authors.initials: M
authors.lastname: Vigier
authors.forename: P
authors.initials: P
authors.lastname: Guillaumot
authors.forename: C
authors.initials: C
authors.lastname: Finaz
mesh_terms: D019326:17-alpha-Hydroxyprogesterone; D015124:8-Bromo Cyclic Adenosine Monophosphate / Q000494:pharmacology; D000311:Adrenal Glands / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology; D000735:Androstenedione / Q000096:biosynthesis; D000818:Animals; D002460:Cell Line; D006063:Chorionic Gonadotropin / Q000494:pharmacology; D000242:Cyclic AMP / Q000096:biosynthesis / Q000494:pharmacology; D003687:Dehydroepiandrosterone / Q000378:metabolism; D015232:Dinoprostone / Q000494:pharmacology; D006822:Hybrid Cells / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D006908:Hydroxyprogesterones / Q000096:biosynthesis; D007985:Leydig Cells / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D011374:Progesterone / Q000378:metabolism; D011388:Prolactin / Q000378:metabolism / Q000494:pharmacology; D013256:Steroids / Q000096:biosynthesis*; D013739:Testosterone / Q000096:biosynthesis; D014660:Vasoactive Intestinal Peptide / Q000494:pharmacology
chemical_list: D006063:Chorionic Gonadotropin; D006908:Hydroxyprogesterones; D013256:Steroids; D015124:8-Bromo Cyclic Adenosine Monophosphate; D014660:Vasoactive Intestinal Peptide; D013739:Testosterone; D000735:Androstenedione; D003687:Dehydroepiandrosterone; D011374:Progesterone; D019326:17-alpha-Hydroxyprogesterone; D000324:Adrenocorticotropic Hormone; D011388:Prolactin; D000242:Cyclic AMP; D015232:Dinoprostone