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Laboratory of Biomedical and Environmental Sciences, Los Angeles 90024 [S. E. W., E. F. H.]; Department of Medicine, University of California, Los Angeles, Los Angeles 90024 [E. F. H.]; and Cancer Center, University of California, San Diego, La Jolla 92093 [C. L. M., L. M.], California
Several well characterized murine T-lymphoma cell lines were used in somatic cell hybridization experiments to study the genetic regulation of glucocorticoid-induced lysis. Cell fusions were carried out among the SL 12-derived cloned lines and between the W7 and SAK8 lines all of which have functional hormone receptors. These cell lines differ in their sensitivity to glucocorticoid-induced lysis. The resultant hybrids were characterized by their growth response to 1 µM dexamethasone, their hormone receptor content, their chromosome number, and the expression of surface antigens. Fusion of the hormone-sensitive W7 parent to a number of glucocorticoid-resistant cell lines resulted in hybrids which were of the sensitive phenotype. In contrast the fusion of another hormone-sensitive clone, SL12.4, with glucocorticoid-resistant SL12 clones or with SAK8 always resulted in hybrids resistant to glucocorticoid lysis. These results reveal a complex genetic regulation of the hormone response or the requirement for multiple gene activity in the mechanism for glucocorticoid-induced cell lysis.
1 The Laboratory of Biomedical and Environmental Sciences is operated for the United States Department of Energy by the University of California under Contract DE-AC03-76-SF00012. This article was supported by the Director of the Office of Energy Research, Office of Health and Environmental Research; NIH Research Grants CA 12386 (U.C.L.A.) and CA 37778 (University of CA, San Diego), and the Margaret E. Early Trust grant.
2 To whom requests for reprints should be addressed, at UCLA Warren Hall, 900 Veteran Avenue, Los Angeles, CA 90024.
Received 3/28/85. Revised 6/10/85. Accepted 6/20/85.
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