RT Journal Article
SR Electronic
T1 A distinct class of plant and animal viral proteins that disrupt mitosis by directly interrupting the mitotic entry switch Wee1-Cdc25-Cdk1
JF Science Advances
JO Sci Adv
FD American Association for the Advancement of Science
SP eaba3418
DO 10.1126/sciadv.aba3418
VO 6
IS 20
A1 Jin, Huaibing
A1 Du, Zhiqiang
A1 Zhang, Yanjing
A1 Antal, Judit
A1 Xia, Zongliang
A1 Wang, Yan
A1 Gao, Yang
A1 Zhao, Xiaoge
A1 Han, Xinyun
A1 Cheng, Yanjun
A1 Shen, Qianhua
A1 Zhang, Kunpu
A1 Elder, Robert E.
A1 Benko, Zsigmond
A1 Fenyvuesvolgyi, Csaba
A1 Li, Ge
A1 Rebello, Dionne
A1 Li, Jing
A1 Bao, Shilai
A1 Zhao, Richard Y.
A1 Wang, Daowen
YR 2020
UL http://advances.sciencemag.org/content/6/20/eaba3418.abstract
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.