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Press release


  • 20 December 2005
  • New discovery in DNA repair gives insights into causes of cancer


     

    An unexpected discovery in the way cells repair damage to their genetic material could improve our understanding of the causes of cancer.

     

    Scientists at the University of Sussex, in collaboration with researchers in Germany and Switzerland, have found that a small protein, ubiquitin, combines with special enzymes in cells to help in repairing DNA, the blueprint for cells.

     

    The ability to deal properly with damaged DNA, either by repairing it or copying it correctly, is an important way in which we are protected against cancer.

     

    "Understanding how this damage can be copied without causing permanent changes or mutations in DNA  gives insights into the causes of cancer," explains Professor Alan Lehmann, chairman of the Genome Damage and Stability Centre at Sussex and co-author of a report published in Science this month  (December).  "This collaborative new study has given us new information on the repair process."

     

    When a DNA strand is damaged, for example by ultraviolet (UV) rays from the sun, the damage hinders the vital process of DNA replication. To get round the lesions, the cell has to employ special enzymes called bypass polymerases.

     

    The scientists have shown that the ability of these polymerases to bind to the protein ubiquitin is crucial for their ability to replicate past the damaged DNA. 

     

    This study provides a long-sought clue on how bypass polymerases succeed in the replication process, when the enzymes that normally copy DNA get stuck at the sites of DNA damage.

     

    The scientists identified two new kinds of structures, or "motifs" in the bypass polymerases called UBM and UBZ, which are found in enzymes that bind ubiquitin. When DNA damage is encountered, a molecule called PCNA (proliferating cell nuclear antigen), a critical factor necessary for replication of DNA, becomes "flagged" by the attachment of a molecule of ubiquitin. The UBM and UBZ motifs enable the bypass polymerases to localize at the sites of DNA damage by preferentially binding to the ubiquitin-flagged PCNA.

     

    The Sussex scientists worked with researchers at Goethe University Medical School in Frankfurt,  Eidgenössische Technische Hochschule (ETHZ) in Zurich, and Miltenyi Biotec in Cologne.

     

    Notes for editors 

    "Ubiquitin-binding domains in Y-family polymerases regulate translesion synthesis" is published in Science ,16 December 2005

     

    University of Sussex press office contacts, Jacqui Bealing or Maggie Clune, Tel: 01273 678888, email: press@sussex.ac.uk

     

     

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