周俭民博士简介

周俭民 博士，高级研究员 Jianmin Zhou, Ph.D., Associate Investigator, National Institute of Biological Sciences, Beijing.
电话（Tel）：010-80726688-8390
传真（Fax）：80726687
E-mail：zhoujianmin@nibs.ac.cn

教育经历Education
1984年 四川大学生物系学士
B.S., Department of Biology, 1984,
Sichuan University, Chengdu, China
1994年 普渡大学园艺学博士
Ph.D., Horticulture, 1994,
Purdue University, USA
研究经历Professional Experience
2004-present National Institute of Biological Sciences, Beijing, China（中国北京生命科学研究所工作）
2002-present Associate Professor of Plant Pathology, Kansas State University（堪 萨斯州立大学植物病理系副教授）
1997-2002 Assistant Professor of Plant Pathology, Kansas State University（堪萨斯州立大学植物病理系助理教授）
1994-1997 Post-Doctoral Associate, Purdue University（普渡大学博士后研究助理）
1989-1994 Doctoral Research Assistant, Purdue University（普渡大学博士生研究助理）
1987-1989 Research Associate, Institute of Genetics, Academia Sinica（中国科学院遗传研究所研究助理）
1984-1987 Master’s Research Assistant, Institute of Genetics, Academia Sinica（中国科学院遗传研究所硕士生研究助理）
研究概述：Research Description
本实验室将致力于植物与微生物间相互作用机理的研究。植物可以感受病原菌的入侵，并且启动防卫反应成功地抵御病原菌的感染。同样，病原菌能够感受植物寄主来激活毒性机制感染寄主，引发病害。在漫长的历史长河中，植物和病原微生物协同进化，抗性机制和毒性机制互相制约。
我们当前的研究主要集中于拟南芥和假单孢杆菌间互作的模式体系。假单孢杆菌包括至少50个不同的pathovar，每个pathovar都有一个特定感染的寄主范围。像其他的很多革兰氏阴性细菌一样，假单孢杆菌通过细菌三型分泌系统将许多效应蛋白直接分泌到寄主细胞。每种病原菌携带一套不同的效应因子, 这些效应因子决定了它们的寄主范围。编码三型分泌系统

及其效应因子的基因受未知的寄主信号激活而表达。在寄主细胞里，这些效应蛋白协同作用而促进病原菌的寄生。然而，我们对这些效应因子在寄主里的靶位点以及病原菌对寄主的致病机制知之甚少。
本实验室主要基于下述方面的研究来阐释植物病理学中的一些基本问题。植物是怎样感受病原菌并激活先天免疫反应的？病原菌是怎样感受寄主并激活其毒性机制的？病原菌寄主范围的决定因素是什么？寄主的免疫机制和病原菌毒性机制是如何相互作用的？
非寄主抗性的研究
此项研究旨在了解非寄主抗性和植物与病原体对寄主的特异性问题。非寄主抗性是对任何植物物种对绝大多数潜在病原菌都具有抗性这一现象的描述(所以也被称之为物种水平抗性)。非寄主抗性是植物最重要最持久的抗性，因而在农业生产中具有极大的应用潜力。但是由于缺乏一个遗传研究系统，目前相关的研究十分欠缺。
我们首次建立了研究植物非寄主抗性的遗传模型。我们的研究结果表明，植物对非寄主病原体的免疫至少部分归功于主动防卫反应。我们已经分离得到了几种对P. s. pv. phaseolicola非寄主抗性有所降低的拟南芥突变系（nho）。NHO1具有对至少三种非寄主病原菌的非特异抗性。有趣的是nho1突变体对于一种应依附于植物的非致病菌——荧光假单孢菌是感病的，然而对于毒性假单孢菌，NHO1似乎并没有起到什么抗性作用。基於这些发现，我们提出了如下假说：NHO1的功能代表一种广谱抗性，但毒性致病菌能利用某种特殊机制克服或者逃避这种抗性。
我们实验室最近分离到了NHO1基因。通过对其表达的分析，我们得以直接验证上述假说。研究发现，非寄主假单孢杆菌菌株能诱导了NHO1基因的转录。令人吃惊的是，毒性致病菌P. s. pv. tomato DC3000能够抑制NHO1基因的转录。这些发现与我们关于NHO1基因的假说完全一致。已有证据表明，在植物体中DC3000通过控制茉莉酮酸的信号通路来抑制NHO1基因的表达。
NHO1基因参与至少四个抗性基因的功能。nho1突变导致这些抗病基因功能的下降。有趣的是，DC3000携带的效应基因avrB诱导而非抑制NHO1基因的表达。avrB激活基因对基因抗性,说明非寄主抗性和基因对基因抗性间存在某种关联。
我们猜测可能是假单孢菌共有的病原相关分子特征（PAMPs）诱导了NHO1基因的表达。毒性致病菌P. s. pv. tomato DC3000能够激活或模仿植物中茉莉酸信号途径来抑制NHO1基因的表达。基因对基因抗性的激活通过作用于茉莉酸信号途径的上游或下游而阻断了这种抑制。这些发现又引出了一系列有趣的问题等待我们去研究，是不是病原相关分子特征激活了

NHO1基因的转录？是什么病原相关分子特征？这些病原相关分子特征是怎样被植物感知的？NHO1基因的诱导机制是什么？毒性病原菌是不是通过三型分泌系统分泌的效应因子来抑制NHO1基因的转录？是什么效应因子在起作用？三型分泌系统分泌的效应因子通过寄主的哪条信号途径来抑制NHO1基因的转录？基因对基因抗性又是怎样参与到先天免疫中去的呢？
调节致病菌基因表达的寄主信号
微生物感受寄主环境的能力对于病原菌的寄生至关重要。微生物通过对植物的感受触发毒性基因或者致病基因的表达，进而抑制、忍受或逃避寄主的防卫反应并得以摄取营养增殖繁衍。
对Ralstonia solanacerum和动物细菌病原体的研究显示，细菌与寄主细胞的直接接触对细菌毒性基因的诱导是必需的。这也说明来自植物细胞的一些非游离性信号与毒性基因或者致病基因的诱导有关。用人工培养基研究发现，某些营养成分和环境因素也能影响致病菌毒性基因的表达。植物来源的信号本质还十分令人费解。
为了进一步了解植物信号的本质，我们利用遗传学方法在拟南芥中鉴定了一个影响致病菌毒性基因表达的遗传位点。拟南芥中遗传位点ATT1能够抑制细菌三型分泌系统基因的表达。ATT1的克隆和对att1突变体进一步鉴定暗示植物细胞外的脂质对抑制细菌三型分泌系统基因的表达和抗病性起一定作用。下一步我们会继续筛选更多的拟南芥突变体，并利用生化方法确定影响细菌三型分泌系统基因表达的各种寄主因子。这些研究会让我们更深刻地了解细菌所感受到的寄主信号。 

My long term interest concerns interactions between plants and pathogenic microbes. Plants are equipped to sense invading phytopathogens and, in most cases, mount successful defense responses to fend off the infection. Likewise, phytopathogens are also capable of sensing the plant to activate virulence mechanisms and cause diseases on their hosts. The resistance mechanisms and virulence mechanisms are intertwined, because they have co-evolved during the long history of plant-pathogen association.
Our current research is focused on the Arabidopsis-Pseudomonas syrinage model.Pseudomonas syringae is comprised of at least 50 different pathovars, each specialized to infect a narrow range of plant species. Like many other Gram-negative bacterial pathogens in plants and animals, Pseudomonas syringae uses the so-called the type III secretion system (also called hrp system) to deliver a repertoire of effector proteins directly into host cells. Each pathovar carries a distinct set of effectors and that is thought to determine its host range. Genes encoding the type III secretion system and effectors are coordinately activated by an undefined host signal. Bacterial effector proteins collectively function inside the host cell to promote parasitism. However, little is known about host targets for these effectors and how they cause diseases.
There are two projects in my laboratory addressing the following fundamental questions in plant biology. How do plants sense pathogens and activate innate immune responses? How do pathogens sense hosts to activate virulence mechanisms? What determines the host range? How do host immunity and pathogen virulence interact?
Nonhost Resistance
A major direction in my laboratory is to understand nonhost resistance and host specificity in plant-pathogen interactions. Nonhost resistance (also called species level resistance) refers to the phenomenon that any given plant species is resistant to the vast majority of potential phytopathogens. It is the most dominant form of resistance in plants. Although it has a great potential in providing crop plants with durable resistance, nonhost resistance is poorly understood because of a lack of genetic systems.
We have established for the first time a genetic model to study nonhost resistance in plants. Our recent results show that immunity to nonhost pathogens is controlled, at least in part, by active defense in plants. We have isolated several Arabidopsis mutants that are compromised in nonhost (nho) resistance to P. syringae pv. phaseolicola. NHO1 is required nonspecifically for resistance to at least three P. syringae pathovars that are nonpathogenic on Arabidopsis. Interestingly, the nho1 mutant also supported the growth of Pseudomonas fluorescens, a plant associating, nonpathogenic bacterium. However, NHO1 does not appear to play a role in the basal resistance to virulent Pseudomonas bacteria. We hypothesized that NHO1 defines a general resistance and that virulent bacteria possess specific mechanisms to overcome/evade this resistance.
The recent cloning and expression studies of NHO1 in our laboratory are allowing us to directly test this hypothesis. NHO1 transcripts are induced by nonhost strains of P. syringae bacteria. Strikingly, NHO1 transcripts are repressed by the virulent bacterium P. syringae pv. tomato DC3000. These findings support the hypothesis that NHO1 is a general resistance gene specifically targeted by bacterial virulence. We have obtained evidence that DC3000 actively manipulates the COI1 ubiquitination pathway in the plant to repress NHO1 expression.
NHO1 is also required for complete gene-for-gene resistance mediated by at least four disease resistance genes, as the nho1 mutation compromised the resistance. Interestingly, DC3000 bacteria 

carrying the avrB gene induces, rather than represses, NHO1 expression. Thus the results demonstrate a link between nonhost resistance and gene-for-gene resistance.
It is likely that Pathogen-Associated Molecular Patterns (PAMPs) shared by Pseudomonas bacteria are responsible for inducing NHO1 expression. The virulent bacterium DC3000 is able to activate or mimic the jasmonic pathway in the plant to repress the NHO1 expression. The activation of gene-for-gene resistance blocks this repression by acting either upstream or downstream of the JA signaling pathway. Our findings raise a number of interesting questions for future research. Do PAMPs activate NHO1 transcription? Which PAMP? How is this PAMP perceived? What is the signal transduction mechanism leading to NHO1 induction? Do virulent bacteria use type III effectors to repress NHO1 transcription? Which effectors? Which host pathway do these type III effectors manipulate to repress NHO1 transcription? How is gene-for-gene resistance integrated into the innate immunity pathway?
Host Signals Involved in Bacterial Gene Expression
The ability of plant-associated microbes to sense the host environment is a crucial step for their successful establishment in plants. Plant-sensing triggers virulence/pathogenicity gene expression, enabling the microbes to suppress, tolerate, or evade host defenses and exploit nutrient for their multiplication.
Studies in Ralstonia solanacerum and animal bacterial pathogens indicate that a physical contact with host cells is required for bacterial virulence gene induction, suggesting that a nondiffusible signal from the plant cell is involved. Studies using artificial media indicated that certain nutrient components and environmental factors also affect the expression of bacterial virulence/pathogenicity genes. The nature of plant-derived signals remains elusive.
In order to gain insight into the nature of the plant signal(s), we have taken a genetic approach to identify genetic loci in Arabidopsis affecting bacterial virulence gene expression. We identified a genetic locus in Arabidopsis, ATT1 (for aberrant induction of type three genes), that suppresses 

type III gene expression in bacteria. The cloning of ATT1 and further characterization of att1 mutants suggested a role of extracellular lipids in inhibiting type III gene expression and disease resistance. Future research will continue the screening for additional att mutants and use biochemical approaches to pinpoint various host factors defined by these mutants. Ultimately these will lead to a better understanding of host signals sensed by thebacterium.
发表文章 Publications:
1. Fangming Xiao, S. Mark Goodwin, Yanmei Xiao, Zhaoyu Sun, Douglas Baker, Xiaoyan Tang, Matthew A. Jenks, and Jian-Min Zhou (2004) Arabidopsis CYP86A2 represses Pseudomonas syringae type III genes and is required for cuticle development. EMBO J., in press.
2. Thara K. Venkatappa, Alexander R. Seilaniantz, Youping Deng, Yinghua Dong, Yinong Yang, Xiaoyan Tang, and Jian-Min Zhou (2004) Tobacco Genes Induced by the Bacterial Effector Protein AvrPto. MPMI, in press.
3. Ping He, Satya Chintamanani, Zhongying Chen, Lihuang Zhu, Barbara N. Kunkel, James R. Alfano, Xiaoyan Tang, and Jian-Min Zhou (2004). Activation of a COI1-dependent pathway in Arabidopsis by Pseudomonas syringae type III effectors and coronatine. The Plant Journal, 37, 589-602.
4. Li Kang, Jianxiong Li, Tiehan Zhao, Fangming Xiao, Xiaoyan Tang, Roger Thilmony, ShengYang He, and Jian-Min Zhou (2003). Interplay of the Arabidopsis nonhost resistance gene NHO1 with bacterial virulence. PNAS, 100, 3519-3524.
5. Jian-Min Zhou and Xiaoyan Tang (2002). Plant disease resistance genes in gene-for-gene resistance and general resistance. In: Andrew J. Wood ed. Biochemical and Molecular Responses of Plants to the Environment, Biochemical & Molecular Responses of Plants to the Environment. Research Signpost, Trivandrum India. pp127. ISBN: 81-7736-167-8.
6. Ping He, Bernd Friebe, Bikram Gill, and Jian-Min Zhou (2003). Allopolyploidy alters gene expression in the highly stable hexaploid wheat. Plant Molecular Biology, 52, 401-414.
7. Thara Venkatappa, John Fellers, and Jian-Min Zhou (2003). In planta induced genes of Puccinia triticina. Molecular Plant Pathology, 4, 51-56.
8. Fangming Xiao, Ming Lu, Tiehan Zhao, Xiaoyan Tang, and Jian-Min Zhou (2003). Pto mutants differentially activate Prf-dependent, AvrPto-independent resistance and gene-for-gene resistance. Plant Physiology, 131, 1239-1249.
9. Jianxiong Li, Libo Shan, Jian-Min Zhou, and Xiaoyan Tang (2002). Overexpression of Pto induces a salicylate-independent cell death but inhibits necrotic lesions caused by salicylate deficiency in tomato plants. MPMI, 15, 654-661.
10. Fang-Ming Xiao, Xiaoyan Tang, and Jian-Min Zhou (2001). Expression of 35S::Pto globally activates defense gene expression in tomato plants. Plant Physiology, 126, 1637-1645.
11. Ping He, Randall F. Warren, Libo Shan, Tiehan Zhao, Lihuang Zhu, Xiaoyan Tang, and Jian-Min Zhou (2001). Overexpression of Pti5 potentiates pathogen-induced defense gene expression in tomato. MPMI 14, 1453-1457.
12. Ming Lu, Xiaoyan Tang, and Jian-Min Zhou. (2001) Arabidopsis NHO1 is required for general resistance against Pseudomonas bacteria. Plant Cell, 13, 437-447.
13. Libo Shan, Venkatappa Thara, Gregory Martin, Jian-Min Zhou, and Xiaoyan Tang (2000). The Pseudomonas AvrPto protein is differentially recognized by tomato and tobacco and is
 

localized to the plant plasma membrane. Plant Cell, 12, 2323-2338.
14. Libo Shan, Ping He, Jian-Min Zhou, and Xiaoyan Tang (2000). A cluster of mutations disrupt the avirulence but not the virulence function of AvrPto. MPMI 13, 592-598.
15. Yong-Qiang Gu, Caimei Yang, Venkatappa Thara, Jian-Min Zhou, and Gregory Martin (2000). Pti4 is induced by ethylene and salicylic acid, and its product is phosphorylated by the Pto kinase. Plant Cell 12, 771-785.
16. Venkatappa K. Thara, Xiaoyan Tang, Gregory B. Martin, and Jian-Min Zhou (1999). Pseudomonas syringae pv tomato induces the expression of tomato EREBP-like genes Pti4 and Pti5 independent of ethylene, salicylate and jasmonate. Plant J. 20, 475-483.
17. Jian-Min Zhou (1999). Signal transduction and pathogen-induced PR gene expression. In: Pathogenesis-related proteins in plants, S.K. Datta and S. Muthukrishnan eds., CRC Press. 195-206.
18. Xiaoyan Tang, Mingtang Xie, Young Jin-Kim, Jian-Min Zhou, Daniel F. Klessig, and Gregory B. Martin (1999). Overexpression of Pto Activates Defense Responses and Confers Broad Resistance. Plant Cell 11: 15-30.
19. Ying-Tsu Loh, Jian-Min Zhou, and Gregory Martin (1998). The myristylation motif of Pto is not required for disease resistance. Mol. Plant-Microbe Interct. 11, 572-576.
20. Ping Xu, Meena Narasimhan, Teresa Samson, Maria Coca, Gyung-Hye Huh, Jian-Min Zhou, Gregory Martin, Paul Hasegawa, and Ray Bressan (1998). A nitrilase-like protein interacts with GCC box DNA-binding proteins involved in ethylene and defense responses. Plant Physiology 118, 867-874.
21. Jian-Min Zhou, Xiaoyan Tang, Reid Frederick, and Gregory Martin (1998). Pathogen recognition and signal transduction by the Pto kinase. J. Plant Res. 111, 353-356.
22. Jian-Min Zhou, Xiaoyan Tang, and Gregory Martin (1997). The Pto kinase conferring resistance to tomato bacterial speck disease interacts with proteins that bind a cis-element of pathogenesis-related genes. EMBO Journal 16, 3207-3218.
23. Yulin Jia, Ying-Tsu Loh, Jian-Min Zhou, and Gregory Martin (1997). Alleles of Pto and Fen occur in bacterial speck-susceptible and fenthion-insensitive tomato lines and encode functional protein kinases. Plant Cell 9, 61-73.
24. Angus Murphy, Jian-Min Zhou, Peter B. Goldsbrough, and Lincoln Taiz (1997). Purification and immunological identification of metallothioneins 1 and 2 from Arabidopsis thaliana. Plant Physiology 113, 1293-1301.
25. Jianjun Chen, Jian-Min Zhou, and Peter B. Goldsbrough (1997). Characterization of phytochelatin synthase from tomato. Physiologia Plantarum 101, 165-172.
26. Martin, G.B., Xiaoyan Tang, Jianmin Zhou, Reid Frederick, Yulin Jia, and Ying-Tsu Loh (1996). Signal recognition and transduction in bacterial speck disease resistance of tomato. In: Biology of Plant-Microbe Interactions, G. Stacey et al. eds. (International Society for Molecular-Microbe Interactions, St. Paul, Minnesota).
27. Martin, G.B., Reid Frederick, Roger L. Thilmony, and Jianmin Zhou (1996). Signal transduction events involved in plant disease resistance. In: Molecular Aspects of Pathogenicity and Resistance: Requirement for Signal Transduction, D. Mills, H. Kunoh, N. T. Keen and S. Mayama eds. U.S./Japan Seminar Series Proceedings, pp. 163-176.
28. Xiaoyan Tang, Reid D. Frederick, Jianmin Zhou, Dennis A. Halterman, Yulin Jia, and Gregory B. Martin (1996). Physical interaction of AvrPto and the Pto kinase defines a
 

recognition event involved in plant disease resistance. Science 274, 2060-2063.
29. Jianmin Zhou, Ying-Tsu Loh, Ray Bressan, and Gregory Martin (1995). The tomato gene Pti1 encodes a serine/threonine kinase that is phosphorylated by Pto and is involved in the hypersensitive response. Cell 83, 925-935.
30. Jianmin Zhou and Peter B. Goldsbrough (1995). Structure, organization and expression of Arabidopsis metallothionein gene family. Mol. Gen. Genet. 248, 318-328.
31. Jianmin Zhou and Peter B. Goldsbrough (1994). Functional homologues of animal and fungal metallothionein genes from Arabidopsis. Plant Cell 6, 875-884.
32. Jianmin Zhou and Peter B. Goldsbrough (1993). An Arabidopsis gene with homology to glutathione s-transferases is regulated by ethylene. Plant Molecular Biology 22, 517-523.
33. Jiaping Zhou, Jianmin Zhou, Sixin Liang, He Huang, Long Pang, and Yinxian Jiao (1990). Cell selection of the tobacco mutant resistant to black shank disease. Acta Genetica Sinica 17(3), 180-188.

INVITED SEMINARS/TALKS
Host factors affecting bacterial gene expression. International Arabidopsis Genome and Proteome Symposium, Hangzhou, May 27, 2004.
Activation and suppression of Arabidopsis innate immune responses. The XIVth International Plant Protection Congress, Beijing, May 15, 2004.
Arabidopsis-Pseudomonas interactions. Yale Biology Meeting, June 7, 2003.
Signaling warfare in plant-bacterial interactions. Institute of Genetics, Chinese Academy ofSciences, Beijing, July, 2002.
In Search of Host Signals and Targets for Pseudomonas Virulence Gene Expression. Ohio State University, February 7, 2002.
Genome specific and nonspecific gene silencing in hexaploid wheat. Polyploidy Workshop, Plant, Animal and Microbe Genomes X Conference, San Diego, 2002.
Arabidopsis defense mutants tell tale of pathogen virulence mechanisms. Purdue University, November 6, 2000.
Arabidopsis NOHHOST1: ancient resistance met by virulence? GPCBC Symposium, Kansas City, September 13-16, 2000.
Genetic analysis of Arabidopsis nonhost resistance to Pseudomonas syringae pv phaseolicola. The 11th International Arabidopsis Conference. Madison, Wisconsin, June, 2000.
Arabidopsis nonhost resistance mechanisms. Workshop “Towards Engineering Signal
Transduction Mechanisms” in: The 6th International Plant Molecular Biology Congress. Quebec, Canada, June, 2000.
Molecular recognition and disease resistance in tomato plants. Department of Biochemistry, Kansas State University, November, 1999.
Molecular basis of gene-for-gene interactions in plants. Department of Plant Pathology, University of Nebraska, October, 1999.
Distinct pathways involved in pathogen-induced expression of the tomato Pti5 gene. Symposium in Plant Hormones: signaling and gene expression. Columbia, Missouri, April, 1999.
Engineering disease resistance: more to learn from plant-pathogen interactions. Grain Marketing and Production Research Center, USDA-ARS, Manhattan, Kansas, April 1999.
Signaling components in the Pto-mediated disease resistance. DuPont Agricultural Products, 

Wilmington, Delaware, April 1997.
Signal perception and transduction by the Pto kinase. The Second European Symposium on Protein Phosphorylation in Plant, Paris, France, April 1997.
Novel approach to engineering disease resistance in plants. Monsanto, St. Louis, Missouri, March 1997.
Early events in the Pto signal transduction pathway: what happens after R gene-avr gene interaction? Department of Plant Pathology, Kansas State University, Manhattan, Kansas, March 1997.
Pto-mediated signal recognition and transduction in disease resistance. Division of Biology, Kansas State University, January 1997.
Signal transduction events of bacterial speck disease resistance in tomato. Department of Horticulture, Purdue University, October 1996.
Pto-mediated signal transduction pathway in disease resistance. Monsanto, St. Louis, Missouri, January 1996.