DNA Repair 2 (2003) 639–652 Meeting Report Report on the First US–Japan DNA Repair Meeting Sendai, Japan, October 27–31, 2002 Errol C. Friedberg a,∗ , Fumio Hanaoka b , Kiyoji Tanaka c , Samuel H. Wilson d , Akira Yasui e a Laboratory of Molecular Pathology, Department of Pathology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9072, USA b Graduate School of Frontier Biosciences, Osaka University, 1-3 Yamada-oka, Suita-shi, Osaka 565-0871, Japan c Human Cell Biology Group, Laboratories for Organismal Biosystems, Graduate School of Frontier Biosciences, Osaka University, 1-3 Yamada-oka, Suita-shi, Osaka 565-0871, Japan d Laboratory of Structural Biology, National Institute of Environmental Health Sciences, NIH, P.O. Box 12233, Research Triangle Park, NC 27709, USA e Department of Molecular Genetics, Institute of Development, Aging and Cancer, Tohoku University, Seiyomachi 4-1, Aoba-Ku, Sendai 980-8575, Japan Received 2 April 2002; accepted 4 February 2003 Joint US–Japan meetings have highlighted scientific exchange and collaboration between the two coun- tries in specific areas of biological research for many years. In late 2002 the first such joint meeting in the field of biological responsiveness to DNA damage was hosted by a Japanese contingent in Sendai, Japan. The meeting 1 was attended by 19 participants from the US and 30 from Japan. The latter included postdoctoral fellows and graduate students from each of the pri- mary Japanese laboratory groups represented at the meeting. It began with an overview of past accom- plishments in the field of biological responsiveness to DNA damage with an emphasis on future prospects for research, presented by Errol Friedberg (University of Texas Southwestern Medical Center at Dallas), who ∗ Corresponding author. Tel.: +1-214-648-4020; fax: +1-214-648-4067. E-mail address: errol.fridberg@utsouthwestern.edu (E.C. Friedberg). 1 This meeting was principally sponsored by the NIEHS, NIH, USA, and by a Grant-in-Aid for Scientific Research on Priority Areas from the Ministry of Education, Culture, Sports, and Science and Technology, Japan. Other sponsors were, ORD, OD, NIH and FIC, NIH. stood in for the indisposed keynote speaker, Philip Hanawalt (Stanford). The following paragraphs sum- marize the remaining oral presentations. Nucleotide excision repair (NER) Kaoru Sugasawa (RIKIN) Kaoru Sugasawa reported that the xeroderma pig- mentosum group C (XPC) protein exists in vivo as a heterotrimeric complex containing HR23B and centrin2. The purified XPC–HR23B heterodimer exhibits specific binding affinity for various base lesions, including (6-4) photoproducts (6-4PP) and N-acetoxy-2-acetylaminofluorene (AAF) adducts. It also binds artificial bubble structures regardless of the presence or absence of lesions, suggesting that the protein does not recognize structural characteristics of the lesions themselves, but rather structural elements of the distorted DNA duplex. The XPC complex prefers specific DNA secondary structures containing a junction with a single-strand tail branching away from duplex DNA in the 3 ′ direction. Since many base lesions handled by NER have been shown to induce DNA helix distortions, including disruption of 1568-7864/03/$ – see front matter doi:10.1016/S1568-7864(03)00038-7