Host: The Japan Radiation Research Society, Chairman of the 52nd Annual Meeting, Toshiteru Okubo (Radiation Effects Research Foundation)
AT (ataxia-telangiectasia) is an autosomal recessive human genetic disorder characterized by radiosensitivity, chromosomal instability, and radioresistant DNA synthesis. The ATDC (AT group D complementing) gene was identified by its ability to restore the radiosensitivity of AT group D cells. Several sizes of ATDC mRNAs have been detected in various cell lines. The ATDC expression is elevated in various cancer tissues and is thought to promote tumor cell proliferation. ATDC is known to be a member of tripartite motif (TRIM) family, which contains a leucine zipper motif and a zinc finger domain. Because the molecular function of ATDC is still unknown, we are trying to establish the cells with ATDC overexpression or the ATDC knockout cell lines.
Overexpression of ATDC partially complemented radiation sensitivity of ATM knockout DT40 cells. This result suggests that ATDC might function in a pathway downstream ATM in response to DNA damage. To examine the role of ATDC in DNA damage repair in ATM deficient cells, ATDC was overexpressed in AT fibroblast carrying SCneo reporter, which can detect homologous recombination repair at a site specific DNA damage. Homologous recombination frequency was not affected by ATDC overexpression, suggesting that ATDC is not directly related to homologous recombination repair of DNA damage. Because ATDC+/- cells showed a significant delay in their cell growth, ATDC might be required for efficient cell proliferation.
