p53 monitors replication fork regression by binding to "Chickenfoot" intermediates

doi:10.1074/jbc.M506348200

HOME

QUICK SEARCH:

	Author:		Keyword(s):
Year:		Vol:		Page:

A more recent version of this article appeared on December 30, 2005

This Article

	Full Text (Accepted Manuscript)
	All Versions of this Article: 280/52/42568 most recent M506348200v1
	Alert me when this article is cited
	Alert me if a correction is posted

Services

	Email this article to a friend
	Similar articles in this journal
	Similar articles in PubMed
	Alert me to new issues of the journal
	Download to citation manager
	Request Permissions

Citing Articles

	Citing Articles via HighWire
	Citing Articles via Google Scholar

Google Scholar

	Articles by Subramanian, D.
	Articles by Griffith, J. D.
	Search for Related Content

PubMed

	PubMed Citation
	Articles by Subramanian, D.
	Articles by Griffith, J. D.

Social Bookmarking

	What's this?

Papers In Press, published online ahead of print October 4, 2005
J. Biol. Chem, 10.1074/jbc.M506348200
Submitted on June 10, 2005
Revised on September 29, 2005
Accepted on October 3, 2005

p53 monitors replication fork regression by binding to "Chickenfoot" intermediates

Deepa Subramanian and Jack D. Griffith

Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599

Corresponding Author: dsubramanian{at}athenixcorp.com

The tumor suppressor protein, p53, utilizes multiple mechanisms to ensure faithful transmission of the genome including regulation of DNA replication, repair and recombination. Monitoring these pathways may involve direct binding of p53 to the DNA intermediates of these processes. In this study, we generated templates resembling stalled replication forks and utilized electron microscopy to examine p53 interactions with these substrates. Our results show that p53 binds with high affinity to the junction of stalled forks whereas two cancer-derived p53 mutants showed weak binding. Additionally, some of the templates were re-arranged to form “chickenfoot” structures in the presence of p53. These were mostly formed due to p53 trapping intermediates of spontaneous fork regression, however, in a small population, the protein appears to be promoting their formation. Collectively, these results demonstrate the importance of sequence-independent binding in p53 mediated maintenance of genomic integrity.

Add to CiteULike CiteULike Add to Complore Complore Add to Connotea Connotea Add to Del.icio.us Del.icio.us Add to Digg Digg Add to Reddit Reddit Add to Technorati Technorati What's this?

This article has been cited by other articles:

S. A. Compton, G. Tolun, A. S. Kamath-Loeb, L. A. Loeb, and J. D. Griffith
The Werner Syndrome Protein Binds Replication Fork and Holliday Junction DNAs as an Oligomer
J. Biol. Chem., September 5, 2008; 283(36): 24478 - 24483.
[Abstract] [Full Text] [PDF]

A. Pamidi, R. Cardoso, A. Hakem, E. Matysiak-Zablocki, A. Poonepalli, L. Tamblyn, B. Perez-Ordonez, M. P. Hande, O. Sanchez, and R. Hakem
Functional Interplay of p53 and Mus81 in DNA Damage Responses and Cancer
Cancer Res., September 15, 2007; 67(18): 8527 - 8535.
[Abstract] [Full Text] [PDF]

N. G. Nossal, A. M. Makhov, P. D. Chastain II, C. E. Jones, and J. D. Griffith
Architecture of the Bacteriophage T4 Replication Complex Revealed with Nanoscale Biopointers
J. Biol. Chem., January 12, 2007; 282(2): 1098 - 1108.
[Abstract] [Full Text] [PDF]

N. Fouche, A. J. Cesare, S. Willcox, S. Ozgur, S. A. Compton, and J. D. Griffith
The Basic Domain of TRF2 Directs Binding to DNA Junctions Irrespective of the Presence of TTAGGG Repeats
J. Biol. Chem., December 8, 2006; 281(49): 37486 - 37495.
[Abstract] [Full Text] [PDF]

N. Fouche, S. Ozgur, D. Roy, and J. D. Griffith
Replication fork regression in repetitive DNAs
Nucleic Acids Res., November 6, 2006; 34(20): 6044 - 6050.
[Abstract] [Full Text] [PDF]