Faculty and Staff
College of Arts and Sciences
|Office:||PSC, Room 717|
|Resources:||Department of Biological Sciences|
Plants provide us with food and essential nutrients. However, many plant pathogens including fungi, oomycetes, bacteria, viruses and nematode cause severe diseases that produce adverse effects on human life. The molecular interactions between pathogens and plants, shaped by millions of years of battle and co-evolution, are a fascinating area of study.
My lab focuses on the plant hormone salicylic acid signaling in plant pathogen interactions. Plant hormone salicylic acid is both required and sufficient for plant defense against biotrophic pathogens. A deeper and more comprehensive understanding of this topic will help us innovate strategies to control plant disease and improve our life quality.
One of the goals in our lab is to increase our understanding of salicylic acid signaling during plant defense against pathogen infection. Specifically, in one of our projects we are investigating how a nuclear kinase contributes to the NPR1 monomer formation and plant defense. NPR1 was identified as a master regulator of plant defense through genetic screens. Before pathogen infections, NPR1 protein mainly exists as oligomers in a resting stage. After pathogen infection, NPR1 oligomers are reduced into monomer and enter nucleus to activate plant defense.
In compatible interactions, virulent plant pathogens win and cause diseases. It would really make sense that plant pathogens would target salicylic acid signaling to disable plant defense. In another project, we are studying how plant bacterial pathogens using type III effectors to modify salicylic acid-mediated plant defense in order to cause diseases.
Fu, Z.Q., and X. Dong. . 2013. Systemic acquired resistance: turning local infection into global defense. Annual Review of Plant Biology. 64: 839-863.
Zheng, X.Y., N. W. Spivey, W. Zeng, P. P. Liu, Z. Q. Fu, D. F. Klessig, N. Zheng and X. Dong. 2012. Coronatine promotes Pseudomonas syringae virulence in plants by activating a signaling cascade that inhibits salicylic acid accumulation. Cell Host Microbe 11. 587-96.
Fu, Z.Q., S. Yan, A. Saleh, W. Wang, J. Ruble, N. Oka, R. Mohan, S. H. Spoel, Y. Tada, N. Zheng, and X. Dong. 2012. NPR3 and NPR4 are receptors for the immune signal salicylic acid in plants. Nature. 486: 228-232.
Block, A., G. Li, Z. Q. Fu, and J.R. Alfano. 2008. Phytopathogen type III effector weaponry and their plant targets. Curr. Opin. Plant Biol. 11: 396-403.
Fu, Z.Q., M. Guo, B. -r. Jeong, F. Tian, T. E. Elthon, R.L. Cerny, D. Staiger, and J. R. Alfano. 2007. A type III effector ADP-ribosylates RNA-binding proteins and quells plant immunity. Nature. 447: 284-288.
Fu, Z.Q., M. Guo, and J.R. Alfano. 2006. The Pseudomonas syringae HrpJ is a type III-secreted protein that is required for plant pathogenesis, injection of effectors, and for secretion of the HrpZ1 harpin. J. Bacteriol. 188: 6060-6069.
Wehling, M. D., M. Guo, Z. Q. Fu, and J. R. Alfano. 2004. The Pseudomonas syringae HopPtoV protein is secreted in culture and translocated into plant cells via the type III protein secretion system in a manner dependent on the ShcV type III chaperone. J. Bacteriol. 186: 3621-30.
Espinosa, A., M. Guo, V. C. Tam, Z. Q. Fu, and J. R. Alfano. 2003. The Pseudomonas syringae type III-secreted protein HopPtoD2 possesses protein tyrosine phosphatase activity and suppresses programmed cell death in plants. Mol. Microbiol. 49: 377-397.