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Differential potency and trans‐activation of normal and mutant T24 human H‐ ras 1 gene promoters
Author(s) -
Spandidos Demetrios A.,
Pintzas Alex
Publication year - 1988
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(88)80751-8
Subject(s) - promoter , microbiology and biotechnology , mutant , biology , transfection , gene , chloramphenicol acetyltransferase , gene expression , transcription (linguistics) , biochemistry , linguistics , philosophy
We have employed a short‐term transfection assay system in which we monitored the transient expression of the chloramphenicol acetyltransferase (CAT) gene linked to the promoter region of the normal and mutant T24 H‐ ras 1 gene or the human ε‐globin gene in Chinese hamster lung (CHL) cells or cells derived from them which carry and express one or the other of the polyoma virus early genes. Our findings can be summarized as follows: (i) The mutant T24 H‐ ras 1 promoter region behaves as a stronger promoter than the H‐ ras 1 gene in all these types of cells as well as in rat 208F fibroblast cells. (ii) In CHL cells expressing the polyoma large T antigen the normal and mutant T24 Ha‐ ras 1 promoters are not trans‐activated in these cells and only a 2.5‐fold activation of the ε‐globin promoter is observed. (iii) In cells expressing the polyoma middle T antigen both the normal and mutant H‐ ras 1 are trans‐activated whereas transcription from the ε‐globin promoter is not affected when compared to the normal CHL cells. (iv) In cells expressing the polyoma small T antigen the normal and mutant H‐ ras 1 as well as the ε‐globin promoters are trans‐activated. We suggest from these data that a tissue‐specific element exists in the promoter region of the H‐ ras 1 gene and that the polyoma middle and small T antigens trigger the expression of proteins that trans‐activate these promoters.