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1 Department of Disease Control, Graduate School of Veterinary Medicine, Hokkaido University, Kita-18, Nishi-9, Kita-ku, Sapporo 060-0818, Japan
2 Department of Microbiology and Immunology, Faculty of Agriculture, Kobe University, 1-1, Rokkodai-cho, Nada-ku, Kobe 657-8501, Japan
Correspondence
Kazuhiko Ohashi
okazu{at}vetmed.hokudai.ac.jp
In tumour cell lines established from Marek's disease (MD) lymphomas L-meq is consistently expressed. It contains a 180 bp insertion encoding additional copies of the proline-rich repeat in the meq open reading frame and its product may contribute to the maintenance of MD virus (MDV) latency. In this study, we identified a novel spliced form of the meq transcript in MD-derived lymphoblastoid cell lines and in MDV-infected cells. This transcript, termed
meq, encodes an N-terminal 98 aa of the Meq protein and lacks part of the basic leucine zipper (bZIP) and transactivation domains. In MD cell lines, transcription of L-meq was significantly downregulated, while that of the
meq transcript was upregulated during apoptosis. These observations were also confirmed at the protein expression level. Reporter assays using meq- and interleukin-2 (IL-2)-promoter-driven luciferase vectors revealed that
Meq suppressed transactivation by L-Meq or Meq in a dose-dependent manner. Immunoprecipitation confirmed that
Meq was associated with L-Meq or Meq physically. These results suggest that
Meq could be involved in apoptosis in MD cell lines as it works as a negative regulator of L-Meq and Meq by direct interaction.
The GenBank/EMBL/DDBJ accession numbers of the sequences reported in this paper are AB091107 (L-meq) and AB091108 (
meq).
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