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Characterization of hydroxyurea resistance in C. elegans

Research output: Contribution to conferencePosterResearch

  • Jeanette Brejning, Denmark
  • Department of Molecular Biology

The soil nematode Caenorhabditis elegans has become a prominent model organism for studying aging and many age-related diseases. We use C. elegans to study the relationship between cancer and aging. To prevent cancer, cells are equipped with surveillance systems that detect damage and stop cells from dividing. These surveillance systems are collectively called cellular checkpoints. We have found that inactivation of certain checkpoint proteins, including p53, also cause resistance to the chemotherapeutic drug hydroxyurea (HU) that stalls replication. We have found that in C. elegans, HU inhibits ribonucleotide reductase (RNR). RNR is involved in synthesis of deoxyribonucleotide (dNTP) precursors for DNA replication and repair.

Previously we have shown that inactivation of some checkpoint proteins can increase stress resistance and lifespan of C. elegans1. Interestingly, several genes that influence HU resistance also influence lifespan and stress resistance. At least one of these genes seems to function in the S-M checkpoint pathway.

  1.    A. Olsen, M. C. Vantipalli, G. J. Lithgow, Science 312, 1381 (2006).  

Original languageEnglish
Publication year2009
Publication statusPublished - 2009
Event17th International C. elegans Meeting - Los Angeles, United States
Duration: 24 Jun 200928 Jun 2009
Conference number: 17


Conference17th International C. elegans Meeting
CountryUnited States
CityLos Angeles

    Research areas

  • checkpoint proteins, hydroxyurea resistance

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