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Bovine leukemia virus trans‐activator p38tax activates heterologous promoters with a common sequence known as a cAMP‐responsive element or the binding site of a cellular transcription factor ATF.
Author(s) -
Katoh I.,
Yoshinaka Y.,
Ikawa Y.
Publication year - 1989
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1002/j.1460-2075.1989.tb03403.x
Subject(s) - biology , chloramphenicol acetyltransferase , promoter , long terminal repeat , bovine leukemia virus , activator (genetics) , regulatory sequence , microbiology and biotechnology , gene , transcription factor , response element , transcription (linguistics) , negative regulatory element , trans acting , gene expression , virus , genetics , mutant , linguistics , philosophy
The genome of bovine leukemia virus (BLV) encodes a transcriptional trans‐activator p38tax (also referred to as pXBL‐I) which amplifies the virus gene expression driven by its long terminal repeat (LTR). It was proposed that activation of cellular gene expression by p38tax might be involved in the mechanism of B‐cell transformation caused in vivo by BLV infection. Here, we report that the U3 region of BLV LTR contains multiple regulatory elements responsive to p38tax. A core element composing the p38tax‐inducible U3 structure is suggested to be a heptanucleotide motif of 5′TGACGTCA3′, the consensus sequence proposed for a cAMP‐responsive element (CRE) and for the binding sites of a cellular transcription factor (ATF). Adenovirus‐5 E3 and E4, c‐fos and somatostatin regulatory regions containing CRE/ATF‐element exhibited responsiveness to p38tax in a chloramphenicol acetyltransferase transient expression assay. These suggest that in BLV‐infected cells, cellular gene expression might be induced abnormally by the virus trans‐activator through ATF or ATF‐like factors.