This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Kajino, K. Articles by Hino, O. Search for Related Content PubMed PubMed Citation Articles by Kajino, K. Articles by Hino, O.

Determination of a Putative Recombinogenic Human Hepatitis B Virus Sequence and Its Binding Cellular Protein¹

Department of Experimental Pathology, Cancer Institute, 1-37-1, Kami-Ikebukuro, Toshima-ku, Tokyo 170 [K. K., O. H.], and Department of Biology, School of Science, Nagoya University, Nagoya 464 [Y. H.], Japan

Previously, we reported that C4BglII196, a 196-base pair subgenomic fragment of hepatitis B virus (HBV) covering its precore region, enhances in vitro recombination in the presence of extracts from actively dividing cells (Hino, O., et al. Proc. Natl. Acad. Sci. USA, 88: 9248–9252, 1991). The results indicated that HBV may play some role in causing genomic instability during chronic hepatitis. In the present study, we showed that 15AB, a 60-base pair subgenomic fragment of HBV DNA (nucleotides 1855–1914) within C4BglII196 is indispensable for enhancement of in vitro recombination, using the mouse leukemia cell 70Z/3, as the cellular extract source. 15AB, thought to be the encapsidation signal of HBV pregenomic RNA and U5-like retrovirus long terminal repeat, was found to bind specifically to an approximately 100 kDa protein of 70Z/3 by southwestern blotting. Production of a mutation in the 15AB region decreased both its binding activity to 100 kDa protein and the in vitro recombination activity. Our present results thus suggest that 15AB might be a recombinogenic sequence and the 100-kDa protein may be a putative recombinogenic protein in eukaryotes, triggering genomic instability and facilitating carcinogenesis.

¹ This work was supported in part by a Grant-in Aid for Cancer Research from the Ministry of Education, Science and Culture of Japan.

² To whom requests for reprints should be addressed.

Received 4/ 8/94. Accepted 6/15/94.