Poster: Late and Moved Abstracts

Abs # 1368: DNA repair and T-DNA transformation: towards gene targeting

Presenter:	Friesner, Joanna D, jdfriesner@ucdavis.edu
Authors	Friesner, Joanna D (A) (C)  Britt, Anne B (A) (B)
Affiliations:	(A): University of California, Davis (B): Section of Plant Biology (C): Genetics Graduate Group

DNA double strand break repair (DSBR) in mammals is of particular interest given its role in the formation of chromosomal deletions. Defects in this repair pathway can also result in translocations or inversions and each of these chromosomal aberrations is commonly seen in cancer and is believed in many cases to be a cause of tumor formation. Genetic analysis of DSBR in mammals is complicated as knockouts in many of the genes are embryonic lethal, triggering a p53-dependent apoptotic pathway. We have shown that mammalian DSBR mechanisms are conserved in plants and that Arabidopsis mutants defective in non-homologous end-joining (NHEJ) homologs of Ku80 and DNA LIGASE IV are viable and normal in the absence of DNA damaging agents. This is significant in that the process of DSBR can be studied in detail without the unwanted side effect of a DNA-damage dependent apoptotic response. The plants are extremely sensitive to ionizing radiation and undergo developmental arrest after treatment. This similarity to mammalian mutants, with the exception of lethality, suggests that Arabidopsis may be an excellent multicellular model for the study of DNA repair. In addition to their role in radiation resistance, Ku80 and DNA LIGASE IV are believed to be involved in the random integration of transgenes into the genome, a process that makes it impossible to efficiently genetically manipulate plants and most other higher eukaryotes. We have shown that while the atku80 and atlig4 mutants are defective in random T-DNA integration, a significant level of integration does occur suggesting that some Ku and LIG4-independent pathway for random transgene integration exists and is fairly efficient in plants.