Plant Programmed Cell Death Caused by an Autoactive Form of Prf Is Suppressed by Co-Expression of the Prf LRR Domain  

作　　者：Xinran Du Min Miao Xinrong Ma Yongsheng Liu Joseph C. Kuhl Gregory B. Martin Fangming Xiao 

机构地区：[1]Department of Plant. Soil and Entomoloqical Sciences, University of Idaho, Moscow, ID 83844. USA [2]Ministry of Education Key Laboratory for Bio-Resource and Eco-Environment, College of Life Science and State Key Laboratory of Hydraulics and Mountain River Engineering, Sichuan University, Chengdu 610064, China [3]Chengdu Institute of Biology, Chinese Academia of Sciences, Chengdu 610064, China [4]School of Biotechnology and Food Engineering, Hefei University of Technology, Hefei 230009, China [5]Boyce Thompson Institute for Plant Research and Department of Plant Pathology and Plant-Microbe Biology, Cornell University, Ithaca, NY 14853, USA

出　　处：《Molecular Plant》2012年第5期1058-1067,共10页分子植物（英文版）

基　　金：the University of Idaho Startup funding to F.X.,the Knowledge Innovation Program of Chinese Academy of Sciences (KSCX2-EW-J-22) to X.M.,the National Science Fund for Distinguished Young Scholars (No.30825030) to Y.L.,and the National Science Foundation grant (DBI-0605059) to G.B.M

摘　　要：In tomato, the NBARC-LRR resistance （R） protein Prf acts in concert with the Pto or Fen kinase to determine immunity against Pseudomonas syringae pv. tomato （Pst）. Prf-mediated defense signaling is initiated by the recognition of two sequence-unrelated Pst-secreted effector proteins, AvrPto and AvrPtoB, by tomato Pto or Fen. Prf detects these inter- actions and activates signaling leading to host defense responses including localized programmed cell death （PCD） that is associated with the arrest of Pst growth. We found that Prf variants with single amino acid substitutions at D1416 in the IHD motif （isoleucine-histidine-aspartic acid） in the NBARC domain cause effector-independent PCD when transiently expressed in leaves of Nicotiana benthamiana, suggesting D1416 plays an important role in activation of Prf. The N-ter- minal region of Prf （NPrf） and the LRR domain are required for this autoactive Prf cell death signaling but dispensable for accumulation of the PrfD1416V protein. Significantly, co-expression of the Prf LRR but not NPrf, with PrfD1416v, AvrPto/Pto, AvrPtoB/Pto, an autoactive form of Pro （PtoY207D）, or Fen completely suppresses PCD. However, the Prf LRR does not in- terfere with PCD caused by Rpi-blblD475v a distinct R protein-mediated PCD signaling event, or that caused by overex- pression of MAPKKKα, a protein acting downstream of Prf. Furthermore, we found the PrfD1416V protein is unable to accumulate in plant cells when co-expressed with the Prf LRR domain, likely explaining the cell death suppression. The mechanism for the LRR-induced degradation of PrfD1416V is unknown but may involve interference in the intramo- lecular interactions of Prf or to binding of the unattached LRR to other host proteins that are needed for Prf stability.In tomato, the NBARC-LRR resistance （R） protein Prf acts in concert with the Pto or Fen kinase to determine immunity against Pseudomonas syringae pv. tomato （Pst）. Prf-mediated defense signaling is initiated by the recognition of two sequence-unrelated Pst-secreted effector proteins, AvrPto and AvrPtoB, by tomato Pto or Fen. Prf detects these inter- actions and activates signaling leading to host defense responses including localized programmed cell death （PCD） that is associated with the arrest of Pst growth. We found that Prf variants with single amino acid substitutions at D1416 in the IHD motif （isoleucine-histidine-aspartic acid） in the NBARC domain cause effector-independent PCD when transiently expressed in leaves of Nicotiana benthamiana, suggesting D1416 plays an important role in activation of Prf. The N-ter- minal region of Prf （NPrf） and the LRR domain are required for this autoactive Prf cell death signaling but dispensable for accumulation of the PrfD1416V protein. Significantly, co-expression of the Prf LRR but not NPrf, with PrfD1416v, AvrPto/Pto, AvrPtoB/Pto, an autoactive form of Pro （PtoY207D）, or Fen completely suppresses PCD. However, the Prf LRR does not in- terfere with PCD caused by Rpi-blblD475v a distinct R protein-mediated PCD signaling event, or that caused by overex- pression of MAPKKKα, a protein acting downstream of Prf. Furthermore, we found the PrfD1416V protein is unable to accumulate in plant cells when co-expressed with the Prf LRR domain, likely explaining the cell death suppression. The mechanism for the LRR-induced degradation of PrfD1416V is unknown but may involve interference in the intramo- lecular interactions of Prf or to binding of the unattached LRR to other host proteins that are needed for Prf stability.

关 键 词：NBARC-LRR resistance protein PRF Pto FEN AvrPto AvrPtoB cell death. 

分 类 号：Q255[生物学—细胞生物学] Q942