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SUMMARY:Controlling Recombination - Simon Boulton\, CRUK Clare Hall Labora
 tories
DTSTART:20110414T151500Z
DTEND:20110414T170000Z
UID:TALK30651@talks.cam.ac.uk
CONTACT:Scientific Meetings Co-ordinator
DESCRIPTION:Unscheduled or excessive homologous recombination (HR) can lea
 d to gross chromosomal rearrangements characteristic of cancer cells\, but
  the mechanisms that restrain HR remained poorly understood. We previously
  reported that rtel-1 mutant worms and RTEL1 depleted human cells exhibit 
 hyper-recombination and sensitivity to DNA damaging agents. Biochemical st
 udies revealed that RTEL1 promotes the disassembly of D loop recombination
  intermediates in vitro\, which led us to propose that RTEL1 acts to count
 eract toxic recombination. More recently\, we have shown that RTEL-1 is re
 quired for crossover interference and homeostasis and promotes non-crossov
 er repair during C. elegans meiosis. Our recent efforts have focused on un
 derstanding the molecular basis of RTEL1 dysfunction in vertebrate cells\;
  loss of Rtel1 results in reduced proliferative capacity\, increased chrom
 atid breaks\, sensitivity to replication blocking lesions and telomere abn
 ormalities. I will present our recent insights into the function of RTEL1 
 in controlling HR at telomeres and the activities that drive telomere dysf
 unction in its absence.
LOCATION:Max Perutz Lecture Theatre\, Medical Research Council (MRC) (MRC 
 Laboratory of Molecular Biol
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