Genome Integrity Discussion Group Meeting
Monday, June 3, 2013
The greater New York Metropolitan area has become a leading center for research on chromosome biology and function, as well as for research at the interface between chromosome integrity and onset and progression of malignancy. The connection between cancer and genome integrity is widely appreciated, and the concentration of excellence in this field is unparalleled anywhere in the world. The Genome Integrity meetings are designed to provide a forum for interactions between the many basic science and clinically-oriented research groups working on these issues. We feel that these interactions will not only facilitate synergy between labs, but also provide a context in which previously unappreciated complementarities will be revealed.
In that spirit, the talks will cover a broad range of areas, including, but not limited to the DNA damage response and cancer predisposition, DNA replication, transcription, chromatin modification, recombination, cell cycle control, telomeres, chromosome segregation, epigenetic states, as well as the emergence of new technologies relevant to research in genome integrity. Although a primary focus is upon basic mechanisms and processes, these areas are pertinent to cancer and myriad human disease states, and it is expected that this will be reflected in the substance of our discussions.
Genome Integrity Discussion Group meetings are organized under the leadership of John Petrini (Memorial Sloan Kettering Cancer Center), and Rodney Rothstein and Lorraine Symington (Columbia University). The year-end meeting includes a scientific symposium with a keynote presentation from 1:00 to 4:00 PM, followed by a poster session and networking reception from 4:00 to 5:30 PM.
|Nonmember (Student / Postdoc / Resident / Fellow)||$20|
The Genome Integrity Discussion Group is proudly supported by
Mission Partner support for the Frontiers of Science program provided by
* Presentation titles and times are subject to change.
Monday June 3, 2013
Keynote address: Defective DNA Strand Break Repair and Links to Human Disease
Coffee break and poster set-up
The role of the LINC complex in the 53BP1-driven mobility and NHEJ of dysfunctional telomeres
Mph1 interplay with nucleases Mus81-Mms4, Yen1 and Rad1-Rad10 to prevent reciprocal translocations between dispersed repeats
Epe1 recruits BET family bromodomain protein Bof1 to establish heterochromatin boundaries
Cell cycle transitions in the absence of nucleosomes
Poster Session and Networking Reception
John Petrini, PhD
Memorial Sloan-Kettering Cancer Center
Rodney Rothstein, PhD
Columbia University Medical Center
Lorraine Symington, PhD
Columbia University Medical Center
Stephen West, PhD
London Research Institute, Cancer Research UK
Stephen West received his PhD in biochemistry from Newcastle University, England, before joining the Department of Therapeutic Radiology at Yale in 1978. There, he was a post-doc with Paul Howard-Flanders, one of the early pioneers in the field of DNA repair. Steve moved back to the UK in 1985 to set up a laboratory at the Imperial Cancer Research Fund (now Cancer Research UK) where he is Senior Group Leader and Deputy Director of Clare Hall Laboratories. Steve's work has focused on the mechanisms of DNA repair by homologous recombination, and the links between repair defects, genome instability and cancer. His early work led to an understanding of homologous pairing by RecA and RAD51, and the resolution of recombination intermediates. Steve discovered the first cellular Holliday junction resolvase (E. coli RuvC), the bacterial branch migration complex (RuvAB), and the human GEN1 Holliday junction resolvase. His work currently revolves around the molecular functions of the BRCA2 tumour suppressor, and the roles and interplay of various Holliday junction resolvases that process recombination intermediates in human cells. Steve has received many awards for his scientific achievements. These include election to EMBO (1994), as a Fellow of the Royal Society (1995), the Academy of Medical Sciences (2000), and the European Academy of Cancer Sciences (2011). He has also received several prizes, including the Swiss Bridge Prize for Cancer Research (2001 and 2009), the Leeuwenhoek Medal of the Royal Society (2002), the Louis-Jeantet Prize for Medicine (2007), the Novartis Medal from the Biochemical Society (2008), the GlaxoSmithKline Medal of the Royal Society (2010), and most recently the Genetics Medal (2012).
de Lange lab, Rockefeller University
Symington lab, Columbia University Medical Center
Jia lab, Columbia University
Christian Zierhut, PhD
Funabiki lab, Rockefeller University
Defective DNA Strand Break Repair and Links to Human Disease
Stephen West, PhD, London Research Institute, Cancer Research UK
The Role of the LINC Complex in the 53BP1-Driven Mobility and NHEJ of Dysfunctional Telomeres
Francisca Lottersberger, PhD, de Lange lab, Rockefeller University
Mph1 Interplay with Nucleases Mus81-Mms4, Yen1 and Rad1-Rad10 to Prevent Reciprocal Translocations between Dispersed Repeats
Gerard Mazón, PhD, Symington lab, Columbia University Medical Center Homology-dependent repair of double-strand breaks (DSBs) from non-sister templates has the potential to generate deleterious genome rearrangements. We show how the Mph1 helicase prevents crossovers between ectopic sequences by removing substrates for Mus81-Mms4 or Rad1-Rad10 cleavage while a role for Yen1 is only detected in the absence of Mus81. Cells lacking Mph1 and the three nucleases are highly defective in the repair a single DSB, suggesting the recombination intermediates that accumulate cannot be processed by the Sgs1-Top3-Rmi1 complex (STR). Consistent with this hypothesis, ectopic joint molecules accumulate transiently in the mph1Δ mutant and persistently when Mus81 is eliminated. Furthermore, the ectopic JMs formed in the absence of Mus81 are connected by a single HJ explaining why STR is unable to process them. We suggest that Mph1 and Mus81-Mms4 recognize a common early strand exchange intermediate and direct repair to non-crossover or crossover outcomes, respectively.
Epe1 Recruits BET Family Bromodomain Protein Bof1 to Establish Heterochromatin Boundaries
Jiyong Wang, PhD, Jia lab, Columbia University
Cell Cycle Transitions in the Absence of Nucleosomes
Christian Zierhut, PhD, Funabiki lab, Rockefeller University
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