Open AccessLoss of DNA-binding and new transcriptionaltransactivation function in polymavirus large T-antigen with mulation of zinc finger motif
Author(s) -
Anders Bergqvist,
Mats Nilsson,
Kåre Bondeson,
Göran Magnusson
Publication year - 1990
Publication title -
nucleic acids research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 9.008
H-Index - 537
eISSN - 1362-4954
pISSN - 0305-1048
DOI - 10.1093/nar/18.9.2715
Subject(s) - zinc finger , biology , mutant , dna , microbiology and biotechnology , transcription (linguistics) , dna binding protein , ring finger domain , dna replication , transcription factor , zinc finger nuclease , gene , biochemistry , linguistics , philosophy
A putative zinc finger in polyomavirus large T-antigen was investigated. We were unable to demonstrate unequivocally a requirement for zinc in specific DNA-binding using the chelating agent 1, 10-phenanthroline. An involvement of the putative zinc finger in specific DNA-binding was nevertheless suggested by the properties of a mutant protein with a cys----ser replacement in the finger motif. Probably as a result of the defective DNA-binding, the mutant protein had lost its activity in initiation of viral DNA-replication and in negative regulation of viral early transcription. However, the trans-activation of the viral late promoter was normal. The analysis also revealed a previously unrecognized activity of large T-antigen. The mutant protein trans-activated the viral early promoter. In the wild-type protein this activity is probably concealed by the separate, negative regulatory function.