TY - JOUR
T1 - A distinct class of plant and animal viral proteins that disrupt mitosis by directly interrupting the mitotic entry switch Wee1-Cdc25-Cdk1
AU - Jin, Huaibing
AU - Du, Zhiqiang
AU - Zhang, Yanjing
AU - Antal, Judit
AU - Xia, Zongliang
AU - Wang, Yan
AU - Gao, Yang
AU - Zhao, Xiaoge
AU - Han, Xinyun
AU - Cheng, Yanjun
AU - Shen, Qianhua
AU - Zhang, Kunpu
AU - Elder, Robert E.
AU - Benko, Zsigmond
AU - Fenyvuesvolgyi, Csaba
AU - Li, Ge
AU - Rebello, Dionne
AU - Li, Jing
AU - Bao, Shilai
AU - Zhao, Richard Y.
AU - Wang, Daowen
N1 - Funding Information:
This work was supported by the Ministry of Science and Technology of China (2017YFD0101000 and 2017YFD0100600 to D.W.) and an intramural start-up fund from Chicago Children’s Memorial Institute of Education and Research, Northwestern University Feinberg School of Medicine and the University of Maryland Medical Center (to R.Y.Z.).
Publisher Copyright:
Copyright © 2020 The Authors.
PY - 2020/5
Y1 - 2020/5
N2 - Many animal viral proteins, e.g., Vpr of HIV-1, disrupt host mitosis by directly interrupting the mitotic entry switch Wee1-Cdc25-Cdk1. However, it is unknown whether plant viruses may use this mechanism in their pathogenesis. Here, we report that the 17K protein, encoded by barley yellow dwarf viruses and related poleroviruses, delays G2/M transition and disrupts mitosis in both host (barley) and nonhost (fission yeast, Arabidopsis thaliana, and tobacco) cells through interrupting the function of Wee1-Cdc25-CDKA/Cdc2 via direct protein-protein interactions and alteration of CDKA/Cdc2 phosphorylation. When ectopically expressed, 17K disrupts the mitosis of cultured human cells, and HIV-1 Vpr inhibits plant cell growth. Furthermore, 17K and Vpr share similar secondary structural feature and common amino acid residues required for interacting with plant CDKA. Thus, our work reveals a distinct class of mitosis regulators that are conserved between plant and animal viruses and play active roles in viral pathogenesis.
AB - Many animal viral proteins, e.g., Vpr of HIV-1, disrupt host mitosis by directly interrupting the mitotic entry switch Wee1-Cdc25-Cdk1. However, it is unknown whether plant viruses may use this mechanism in their pathogenesis. Here, we report that the 17K protein, encoded by barley yellow dwarf viruses and related poleroviruses, delays G2/M transition and disrupts mitosis in both host (barley) and nonhost (fission yeast, Arabidopsis thaliana, and tobacco) cells through interrupting the function of Wee1-Cdc25-CDKA/Cdc2 via direct protein-protein interactions and alteration of CDKA/Cdc2 phosphorylation. When ectopically expressed, 17K disrupts the mitosis of cultured human cells, and HIV-1 Vpr inhibits plant cell growth. Furthermore, 17K and Vpr share similar secondary structural feature and common amino acid residues required for interacting with plant CDKA. Thus, our work reveals a distinct class of mitosis regulators that are conserved between plant and animal viruses and play active roles in viral pathogenesis.
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U2 - 10.1126/sciadv.aba3418
DO - 10.1126/sciadv.aba3418
M3 - Article
C2 - 32426509
AN - SCOPUS:85084787174
SN - 2375-2548
VL - 6
JO - Science Advances
JF - Science Advances
IS - 20
M1 - eaba3418
ER -
