ArticleJournal of virology2003
Nonspecific double-stranded DNA binding activity of simian virus 40 large T antigen is involved in melting and unwinding of the origin.
Article in Journal of virology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- Viral DNA replication-dependent DNA damage response activation during BK polyomavirus infection.Journal of virology · 2015Article
- Translocation and stability of replicative DNA helicases upon encountering DNA-protein cross-links.The Journal of biological chemistry · 2013Article
- Large T antigen promotes JC virus replication in G2-arrested cells by inducing ATM- and ATR-mediated G2 checkpoint signaling.The Journal of biological chemistry · 2010Article
- Simian virus 40 large T antigen can specifically unwind the central palindrome at the origin of DNA replication.Journal of virology · 2009Article
- Systematic study of the functions for the residues around the nucleotide pocket in simian virus 40 AAA+ hexameric helicase.Journal of virology · 2008Article
- Simian virus 40 DNA replication is dependent on an interaction between topoisomerase I and the C-terminal end of T antigen.Journal of virology · 2008Article
- Quantitative analysis of the binding of simian virus 40 large T antigen to DNA.Journal of virology · 2007Article
- Role of the hydrophilic channels of simian virus 40 T-antigen helicase in DNA replication.Journal of virology · 2007Article
- Model for T-antigen-dependent melting of the simian virus 40 core origin based on studies of the interaction of the beta-hairpin with DNA.Journal of virology · 2007Article
- The roles of the residues on the channel beta-hairpin and loop structures of simian virus 40 hexameric helicase.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- Epigenetic mechanisms affect mutant p53 transgene expression in WAP-mutp53 transgenic mice.Oncogene · 2005Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Helicase activity is required for T antigen to unwind the simian virus 40 origin. We previously mapped this activity to residues 131 and 616. In this study, we generated a series of mutants with single-point substitutions in the helicase domain to discover other potential activities required for helicase function. A number of DNA unwinding-defective mutants were generated. Four of these mutants (456RA, 460ED, 462GA, and 499DA) were normal in their ability to hydrolyze ATP and were capable of associating into double hexamers in the presence of origin DNA. Furthermore, they possessed normal ability to bind to single-stranded DNA. However, they were severely impaired in unwinding origin-containing DNA fragments and in carrying out a helicase reaction with an M13 partial duplex DNA substrate. Interestingly, these mutants retained some ability to perform a helicase reaction with artificial replication forks, indicating that their intrinsic helicase activity was functional. Intriguingly, these mutants had almost completely lost their ability to bind to double-stranded DNA nonspecifically. The mutants also failed to melt the early palindrome region of the origin. Taken together, these results indicate that the mutations have destroyed a novel activity required for unwinding of the origin. This activity depends on the ability to bind to DNA nonspecifically, and in its absence, T antigen is unable to structurally distort and subsequently unwind the origin.
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