董欣年

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董欣年,女,美国分子生物学、植物生理学家,1959年出生于湖北省武汉市[1]  ,籍贯浙江省宁波市。杜克大学生物学系教授。2012年获选美国科学院院士[2] 
中文名
董欣年
出生地
湖北省武汉市
出生日期
1959年
职    业
美国分子生物学、植物生理学家
主要成就
2012年获选美国科学院院士
籍    贯
浙江省宁波市

董欣年人物经历

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董欣年1978年考入武汉大学生物学系,1982年,获武大学士。参加首届“中美生物化学联合招生项目”(CUSBEA,发起人为吴瑞教授),获得留美资格。丈夫王小凡为在同届CUSBEA考试中获得第一名。夫妻双双留学美国。
1983年至1988年,就读于美国西北大学(位于芝加哥),获得分子生物学理学博士。1988至1991年,在哈佛大学医学院从事博士后研究。
1992年起,历任杜克大学生物系助理教授、副教授、教授。

董欣年个人生活

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董欣年教授籍贯是浙江宁波,出身于学术世家。父亲是有“一代经济学泰斗”之称的董辅礽[3]  。母亲刘蔼年,是中国著名眼科医生、教授。一家都是武汉大学校友。其中董辅礽1946年毕业于国立武汉大学,后来成为武大教授和经济系主任。母亲刘氏[4]  1949年毕业于武大,曾是解放军海军总医院眼科主任。有弟董欣中,美国约翰霍普金斯大学神经生物学教授。丈夫王小凡,是董欣年在武大的同学,与董欣年同为杜克大学教授,任教于药理系。

董欣年研究领域

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主要研究领域为植物分子生物学和生理学,特别是水杨酸茉莉酸在植物细胞内和体内的信号转导途径,及其相互作用的机制。

董欣年论文专著

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Specialties:
Cell and Molecular Biology
Genetics
Genomics
Research Categories: Plant-Microbe interactions
Current projects: (1) Functional analysis of NPR1, a positive regulator of SAR, (2) Functional analysis of SNI1, a negative regulator of SAR, (3) Study of cross-talks between different defense pathways, (4) Study of programmed cell death in plant defense, (5) Expression profiling of plant defense responses, (6) Study of protein secretory pathway in plant defense, (7) Characterization of antifungal proteins in seeds
Research Description: Using Arabidopsis thaliana as a model system, my laboratory studies the mechanisms of plant defense against microbial pathogens. We focus on a specific response known as systemic acquired resistance (SAR). SAR, which can be induced by a local infection, provides the plants with long lasting, systemic resistance against a broad spectrum of pathogens. Salicylic acid (SA; an active ingredient of aspirin) has been found to be the endogenous signal of SAR. Using a genetic approach, our laboratory identified genes involved in the regulation of SAR. Molecular and genetic analyses are being carried out to understand the gene function and to elucidate the SAR signaling pathway. These SAR-regulating genes are also favorite targets for molecular engineering of disease-resistance crops.
Areas of Interest:
signaling transduction mechanisms
plant-microbe interaction
regulation of gene expression
functional genomics
Representative Publications (More Publications) (search)
Wang, W., Barnaby, J. Y., Tada, Y., Li, H., Tör, M., Caldelari, D., Lee, D.-u. Fu, X.-D. and Dong, X.,Timing of plant immune responses by a central circadian regulator, Nature, vol. 470 (2011), pp. 110–114 .
Wang, S., Durrant, W. E., Song, J., Spivey, N. W., and Dong X., The Arabidopsis BRCA2 and RAD51 proteins are specifically involved in defense gene transcription during plant immune responses., Proc. Natl. Acad. Sci. USA (2010) [doi] .
SH Spoel, Z Mou, Y Tada, NW Spivey, P Genschik, X Dong, Proteasome-mediated turnover of the transcription coactivator NPR1 plays dual roles in regulating plant immunity., Cell, vol. 137 (May, 2009), pp. 860-72 [abs].
Tada, Y., Spoel, S. H., Pajerowska-Mukhtar, K., Mou Z., Song, J., Dong, X., Plant Immunity Requires Conformational Changes of NPR1 via S-Nitrosylation and Thioredoxins, Science (2008) [8he5p3s6CA6g&keytype=ref&siteid=sci] [abs].
Dong, W., Weaver, N.D., Kesarwani, M., Dong, X., Induction of Protein Secretory Pathway Is Required for Systemic Acquired Resistance, Science, vol. 308 (2005), pp. 1036-1040 .
Mou, Z. Fan, W., and Dong, X., Inducers of plant systemic acquired resistance regulate NPR1 function through redox changes., Cell, vol. 113 (2003), pp. 935 .
Durrant, W. E., and Dong, X., Systemic acquired resistance, Annual Review of Phytopathology, vol. 42 (2004), pp. 185-209 .
Li, X., Zhang, Y., Clarke, J.D., Li, Y., and Dong, X, Identification and cloning of a negative regulator of systemic acquired resistance, SNI1, through a screen for suppressors of npr1-1, Cell, vol. 98 (1999), pp. 329 .
Kinkema, M., Fan, W., and Dong, X., Nuclear localization of NPR1 is required for activation of PR gene expression, Plant Cell, vol. 12 (2000), pp. 2339-2350 .
Zhang, Y., Fan, W., Kinkema, M., Li, Xin, and Dong, X, Interaction of NPR1 with basic leucine zipper protein transcription factors that bind sequences required for salicylic acid induction of the PR-1 gene., Proc. Natl. Acad. Sci. USA, vol. 96 (1999), pp. 6523 .
Clarke, J.D., Volko, S.M., Ledford, H., Ausubel, F.M., and Dong, X., Roles of salicylic acid, jasmonic acid, and ethylene in cpr-induces resistance in Arabidopsis, Plant Cell, vol. 12 (2000), pp. 2175-2190 .
Cao, H., X. Li, and X. Dong, Generation of broad-spectrum disease resistance by overexpression of an essential regulatory gene in systemic acquired resistance., Proc. Natl. Acad. Sci. USA, vol. 95 (1998), pp. 6531-6536 .
Cao, H., J. Glazebrook, J. D. Clarke, S. Volko, and X. Dong., The Arabidopsis NPR1 gene that controls systemic acquired resistance encodes a novel protein containing ankyrin repeats., Cell, vol. 88 (1997), pp. 57-63 .
Cao, H., S. A. Bowling, A. S. Gordon, and X. Dong, Characterization of an Arabidopsis mutant that is nonresponsive to inducers of systemic acquired resistance., Plant Cell, vol. 6 (1994), pp. 1583-1592 .
Durrant, W. E., Wang, S., Dong, X., Arabidopsis SNI1 and RAD51D regulate both gene transcription and DNA recombination during the defense response., PNAS USA, vol. 104 no. 10 (2007), pp. 4223-7 [abs].
D Wang, K Pajerowska-Mukhtar, AH Culler, X Dong, Salicylic acid inhibits pathogen growth in plants through repression of the auxin signaling pathway., Current biology : CB, England, vol. 17 no. 20 (October, 2007), pp. 1784-90 [abs].
Wang, D., Amornsiripanitch, N., Dong, X., A genomic approach to identify regulatory nodes in the transcriptional network of systemic acquired resistance in plants, PloS Pathogens, vol. 2 (2006), pp. 1042-1050 .
SH Spoel, JS Johnson, X Dong, Regulation of tradeoffs between plant defenses against pathogens with different lifestyles., Proceedings of the National Academy of Sciences of the United States of America, United States, vol. 104 no. 47 (November, 2007), pp. 18842-7 [abs].
A. Heidel, J. D. Clarke, J. Antonovics, and X. Dong, Fitness costs of mutants affecting the systemicacquired resistance pathway in Arabidopsis thaliana, Genetics, vol. 168 (2004), pp. 2197-2206 .
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