Open AccessMutations in the bovine leukemia virus Tax protein can abrogate the long terminal repeat-directed transactivating activity without concomitant loss of transforming potential.
Author(s) -
Lucas Willems,
Catherine Grimonpont,
Hubertine Heremans,
Nicole Rebeyrotte,
Guangling Chen,
Daniel Portetelle,
Arsène Burny,
Richard Kettmann
Publication year - 1992
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.89.9.3957
Subject(s) - transactivation , long terminal repeat , zinc finger , biology , bovine leukemia virus , gene , virus , microbiology and biotechnology , genetics , gene expression , transcription factor
The bovine leukemia virus Tax protein transactivates gene expression directed by the viral long terminal repeat (LTR) and contributes to immortalization of primary cells. Theoretical analysis of the protein sequence revealed the presence of a putative zinc finger structure at its amino end. Selected mutations in that region completely abolished transactivation, demonstrating its importance for LTR-directed gene regulation. However, these mutations did not interfere with the ability of tax to bind zinc or to contribute to immortalization of primary cells. Thus, transactivation of bovine leukemia virus LTR and target cell transformation are independent functions of Tax and involve different functional domains of the protein.