Mitochondrial Location of Severe Acute Respiratory Syndrome Coronavirus 3b Protein

  • Yuan, Xiaoling (Department of Pathophysiology, Beijing Institute of Radiation Medicine) ;
  • Shan, Yajun (Department of Pathophysiology, Beijing Institute of Radiation Medicine) ;
  • Yao, Zhenyu (Department of Pathophysiology, Beijing Institute of Radiation Medicine) ;
  • Li, Jianyong (Department of Pathophysiology, Beijing Institute of Radiation Medicine) ;
  • Zhao, Zhenhu (Department of Pathophysiology, Beijing Institute of Radiation Medicine) ;
  • Chen, Jiapei (Department of Pathophysiology, Beijing Institute of Radiation Medicine) ;
  • Cong, Yuwen (Department of Pathophysiology, Beijing Institute of Radiation Medicine)
  • Received : 2005.06.03
  • Accepted : 2005.12.26
  • Published : 2006.04.30

Abstract

Severe acute respiratory syndrome-associated coronavirus (SARS-CoV), a distant member of the Group 2 coronaviruses, has recently been identified as the etiological agent of severe acute respiratory syndrome (SARS). The genome of SARS-CoV contains four structural genes that are homologous to genes found in other coronaviruses, as well as six subgroup-specific open reading frames (ORFs). ORF3 encodes a predicted 154-amino-acid protein that lacks similarity to any known protein, and is designated 3b in this article. We reported previously that SARS-CoV 3b is predominantly localized in the nucleolus, and induces G0/G1 arrest and apoptosis in transfected cells. In this study, we show that SARS-CoV 3b fused with EGFP at its N- or C- terminus co-localized with a mitochondriaspecific marker in some transfected cells. Mutation analysis of SARS-CoV 3b revealed that the domain spanning amino acids 80 to 138 was essential for its mitochondria localization. These results provide new directions for studies of the role of SARS-CoV 3b protein in SARS pathogenesis.

Keywords

References

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