Genetic analysis of dexamethasone resistance in L cells by somatic cell hybridization.
Stable dexamethasone resistant and receptor-containing (R+) variants of L cells have been characterized by somatic cell hybridization. Neither of the variants had a clearly dominant phenotype in hybrids with dexamethasone-sensitive fibroblast lines, i.e. the resistance of the variants was not due to transdominant factors. Somatic cell hybrids formed between one of the R+-resistant clones and an independent resistant fibroblast cell line showed complementation--the hybrid clones were as sensitive to the steroid as the sensitive parental lines. Complementation, however, disappeared after continued culture of the clones. The return of the dexamethasone-sensitive phenotype was not always linked with similar changes in the responsiveness to another steroid, e.g. progesterone. Our clones can be considered to be resistant variants, designated death-less (d-), where the cells are defective in a non-receptor component involved in the hormone response. The fact that complementation can occur indicates the existence of at least two such steps in the pathway.
D000818:Animals; D002455:Cell Division / Q000187:drug effects; D002460:Cell Line; D003907:Dexamethasone / Q000494:pharmacology*; D004351:Drug Resistance; D005347:Fibroblasts / Q000187:drug effects*; D006822:Hybrid Cells / Q000187:drug effects*; D051379:Mice; D010641:Phenotype; D011397:Promegestone / Q000494:pharmacology; D011965:Receptors, Glucocorticoid / Q000378:metabolism; D011980:Receptors, Progesterone / Q000378:metabolism; D013936:Thymidine / Q000378:metabolism
D011965:Receptors, Glucocorticoid; D011980:Receptors, Progesterone; C028697:dexamethasone receptor; D003907:Dexamethasone; D011397:Promegestone; D013936:Thymidine