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PARENT SESSION

Genomic Maintenance & Repair

Monday, October 17, 2005 3:00 PM-5:00 PM Exhibit Hall

(PP309) Deletion of mouse Rad9 leads to high spontaneous frequencies of sister chromatid exchange.

Hopkins, Kevin*,1, Balajee , Adayabalam1, Lieberman, Howard1, 1 Center for Radiological Research, New York, NY

ABSTRACT- We generated mouse embryonic stem cells deleted for Mrad9 to determine the role of the gene in the response of cells to DNA damaging agents. We found that these cells are very sensitive to a number of DNA damaging agents including gamma rays, ultraviolet light, hydroxyurea, and mitomycin C. To understand the function of Mrad9 in promoting cell survival after exposure to these DNA damaging agents, we initiated a study to examine the role of the protein in homologous recombination. To do this, we started by determining the spontaneous level of sister chromatid exchange (SCE) in cells differing in the status of Mrad9, including populations that were Mrad9+/+, Mrad9+/-, Mrad9-/-, and the latter ectopically expressing HRAD9 or Mrad9. We found that cells null for Mrad9 have a two-fold increase in the spontaneous level of SCE, relative to wild-type Mrad9 cells. This higher level was reflected both in terms of exchanges per cell and per chromosome. In addition, the range of SCEs per cell for the Mrad9+/+ population was 1-16, whereas the range for Mrad9-/- was 4-24. Additional studies are underway to understand how mutations in Mrad9 lead to the formation of high levels of SCEs, and how these results relate to cellular resistance to DNA damage.

Key words: Rad9, homologous recombination, sister chromatid exchange, DNA repair


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2005 RRS