한빛사논문
Mazen Alazem,1,2,*,† John Bwalya,3 Pai Hsuan,4 Jisuk Yu,1 Huong Cam Chu,3 Tessa Burch-Smith 2 and Kook-Hyung Kim 1,3,5,*
1Plant Genomics and Breeding Institute, Seoul National University, Seoul 08826, Republic of Korea
2The Donald Danforth Plant Science Center, St. Louis, MO 63132, USA
3Department of Agricultural Biotechnology, College of Agriculture and Life Sciences, Seoul National University, Seoul 08826, Republic of Korea
4The Sainsbury Laboratory, University of East Anglia, Norwich 08826, UK
5Research Institute of Agriculture and Life Sciences, Seoul National University, Seoul 08826, Republic of Korea
*Corresponding author: correspondence to Mazen Alazem or Kook-Hyung Kim
†Present address: The Donald Danforth Plant Science Center, St. Louis, MO 63132, USA.
Abstract
Viral synergism occurs when mixed infection of a susceptible plant by 2 or more viruses leads to increased susceptibility to at least 1 of the viruses. However, the ability of 1 virus to suppress R gene-controlled resistance against another virus has never been reported. In soybean (Glycine max), extreme resistance (ER) against soybean mosaic virus (SMV), governed by the Rsv3 R-protein, manifests a swift asymptomatic resistance against the avirulent strain SMV-G5H. Still, the mechanism by which Rsv3 confers ER is not fully understood. Here, we show that viral synergism broke this resistance by impairing downstream defense mechanisms triggered by Rsv3 activation. We found that activation of the antiviral RNA-silencing pathway and the proimmune mitogen-activated protein kinase 3 (MAPK3), along with the suppression of the proviral MAPK6, are hallmarks of Rsv3-mediated ER against SMV-G5H. Surprisingly, infection with bean pod mottle virus (BPMV) disrupted this ER, allowing SMV-G5H to accumulate in Rsv3-containing plants. BPMV subverted downstream defenses by impairing the RNA-silencing pathway and activating MAPK6. Further, BPMV reduced the accumulation of virus-related siRNAs and increased the virus-activated siRNA that targeted several defense-related nucleotide-binding leucine-rich repeat receptor (NLR) genes through the action of the suppression of RNA-silencing activities encoded in its large and small coat protein subunits. These results illustrate that viral synergism can result from abolishing highly specific R gene resistance by impairing active mechanisms downstream of the R gene.
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