BIOC/MCB 568 -- Fall 2010
John W. Little--University of ArizonaBIOC/MCB568 Home Page
Note: Most of the links given here are to PubMed pages; from University computers, there should be a link near the top of the page to the article itself. If there is no link, you can usually get there from the Science Library Biochem Journals link. Some links here are to the articles themselves; these can be accessed from University computers, or from your home computer if you have VPN installed on it.
Friedberg, E.C. Nat. Rev. Mol. Cell Biol. 6, 943-953 (2005). "Suffering in silence: The tolerance of DNA damage." Distributed in class.
Friedberg, E.C. Nature 421, 436-440 (2003). "DNA damage and repair." A more historical perspective on this field.
Friedberg, E.C., Lehmann, A.R. and Fuchs, R.P.P. Mol Cell 18, 499-505 (2005). "Trading places: How do DNA polymerases switch during translesion DNA synthesis?"
Langston, L.D. and O'Donnell, M. Mol. Cell 23, 155-160 (2006). "DNA replication: Keep moving and don't mind the gap." Reviews evidence that the replication fork can pass sites of damage without stalling, by making new primers downstream of the damage. This can happen on the leading strand.
Heller, R.C. and Marians, K.J. Nat. Rev. Mol. Cell Biol. 7, 932-943 (2006). "Replisome assembly and the direct restart of stalled replication forks." Discusses diverse mechanisms for repairing and restarting stalled forks.
Yang, W. and Woodgate, R. PNAS 104, 15591-15598 (2007). "What a difference a decade makes: Insights into translesion synthesis." Focuses on insights gained from x-ray crystallography.
Yang, W. Cell Research 18, 184-197 (2008). "Structure and mechanism for DNA lesion recognition." Focuses on structural analysis of proteins involved in recognizing and repairing lesions.
Li, X. and Heyer, W. Cell Research 18, 99-113 (2008). "Homologous recombination in DNA repair and DNA damage tolerance."
Yao, N.Y. and O'Donnell, M. Curr.Op. in Cell Biology 21, 336-343 (2009). "Replisome structure and conformational dynamics underlie fork progression past obstacles."
Tang, M., Bruck, I. Eritja, R. Turner, J., Frank, E.G., Woodgate, R., O'Donnell, M. and Goodman, M.F. PNAS 95, 9755-9760 (1998). "Biochemical basis of SOS-induced mutagenesis in Escherichia coli: Reconstitution of in vitro lesion bypass dependent on the UmuD'2C mutagenic complex and RecA protein".
Tang, M., Shen, X., Frank, E.G., O'Donnell, M., Woodgate, R. and Goodman, M.F. PNAS 96, 8919-8924 (1999). "UmuD'2C is an error-prone DNA polymerase, Escherichia coli pol V." Follow-up paper to the previous one.
Schlacher, K., Cox, M.M., Woodgate, R. and Goodman, M.F. Nature 442, 883-887 (2006). "RecA acts in trans to allow replication of damaged DNA by DNA polymerase V".
Heller, R.C. and Marians, K.J. Nature 439, 557-562 (2006). "Replication fork reactivation downstream of a blocked nascent leading strand". Evidence that primers can be made downstream of a block on the leading strand.
Link to a web page on the class site: "Interconversion of various forms of the Holliday junction, fork reassembly after fork hits a nick, DSB repair model, more on RecA. Relevant both to repair and to recombination.
http://www.biochem.arizona.edu/classes/bioc568/bioc568.htm
Last modified September 10, 2010
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