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Journal of Virology, March 2000, p. 2636-2646, Vol. 74, No. 6
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Genetic Studies with the Fission Yeast Schizosaccharomyces pombe Suggest Involvement of Wee1, Ppa2, and Rad24 in Induction of Cell Cycle Arrest by Human Immunodeficiency Virus Type 1 Vpr

Michiaki Masuda,1,* Yukiko Nagai,1 Norihito Oshima,1 Koichi Tanaka,2 Hiroshi Murakami,2 Hiroko Igarashi,1 and Hiroto Okayama2

Department of Microbiology1 and Department of Biochemistry and Molecular Biology,2 Graduate School of Medicine, The University of Tokyo, Tokyo 113-0033, Japan

Received 3 September 1999/Accepted 8 December 1999

Accessory protein Vpr of human immunodeficiency virus type 1 (HIV-1) arrests cell cycling at G2/M phase in human and simian cells. Recently, it has been shown that Vpr also causes cell cycle arrest in the fission yeast Schizosaccharomyces pombe, which shares the cell cycle regulatory mechanisms with higher eukaryotes including humans. In this study, in order to identify host cellular factors involved in Vpr-induced cell cycle arrest, the ability of Vpr to cause elongated cellular morphology (cdc phenotype) typical of G2/M cell cycle arrest in wild-type and various mutant strains of S. pombe was examined. Our results indicated that Vpr caused the cdc phenotype in wild-type S. pombe as well as in strains carrying mutations, such as the cdc2-3w, Delta cdc25, rad1-1, Delta chk1, Delta mik1, and Delta ppa1 strains. However, other mutants, such as the cdc2-1w, Delta wee1, Delta ppa2, and Delta rad24 strains, failed to show a distinct cdc phenotype in response to Vpr expression. Results of these genetic studies suggested that Wee1, Ppa2, and Rad24 might be required for induction of cell cycle arrest by HIV-1 Vpr. Cell proliferation was inhibited by Vpr expression in all of the strains examined including the ones that did not show the cdc phenotype. The results supported the previously suggested possibility that Vpr affects the cell cycle and cell proliferation through different pathways.

* Corresponding author. Mailing address: Department of Microbiology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan. Phone: 81-3-5841-3409. Fax: 81-3-5841-3374. E-mail: mmasuda{at}m.u-tokyo.ac.jp.

Journal of Virology, March 2000, p. 2636-2646, Vol. 74, No. 6
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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