Characterization of Negative Regulators of NPR1-Mediated Systemic Acquired Resistance
Characterization of Negative Regulators of NPR1-Mediated Systemic Acquired Resistance
批准号:
0090887
负责人:
Xinnian Dong
金额:
$52.0万
依托单位:
依托单位国家:
美国
项目类别:
Continuing Grant
财政年份:
2001
资助国家:
美国
项目状态:
已结题
起止时间:
2001-02-15 至 2006-01-31
中文摘要
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英文摘要
The long-term goal of this research is to use Arabidopsis thaliana as amodel system to determine the signaling events leading to systemic acquiredresistance (SAR). SAR is a secondary pathogen resistance which can beinduced after a local infection. SAR is broad-spectrum and long-lasting.Through genetic screens, NPR1 has been identified as a key positiveregulator of SAR; mutants of the NPR1 gene are nonresponsive to SARinduction. NPR1 encodes a novel protein with functionally importantprotein-protein interacting domains, the BTB domain and the ankyrin-repeatdomain. Recent data show that nuclear localization of NPR1 is essentialfor its function. In the nucleus, NPR1 may affect the activities of theTGA subclass of bZIP transcription factors as well as the WRKYtranscription factors, which have been implicated as transcriptionalactivators and repressors of pathogenesis-related (PR) genes, respectively.A genetic screen for suppressors of npr1 has led to identification of sni1,a mutation that restores systemic induction of PR genes in npr1. Thewild-type SNI1 is believed to be a negative regulator of SAR whoseinactivation requires the function of NPR1. It is hypothesized that NPR1induces SAR by activating the TGA transcription activators and inactivatingWRKY transcription repressors, and relieving the negative control of SNI1.In this project, molecular genetic and biochemical experiments are designedto (1) determine the functional significance of the interaction betweenNPR1 and WRKY transcription factors in SAR; (2) determine the mechanism bywhich SNI1 functions as a negative regulator of SAR; and (3) identifycomponents in the NPR1-complex. Because NPR1, SNI1, and WRKY transcriptionfactors are either novel or plant-specific proteins, characterization ofthese components may unveil new mechanisms of signal transduction.Understanding molecular mechanisms of disease resistance in plants willlead to the development of technology in enhancing plants' innate defenseto control infection. Such technology has the potential to reduce the useof hazardous pesticides without using non-plant genes. Therefore, thestudy of plant-microbe interactions is of interest to advancement of basicscience as well as to protection of the environment and improvement ofhuman life.
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批准号:2041378
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资助金额:$100.0万
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批准号:1745595
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资助金额:$5.0万
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CONFERENCE: The 22nd International Conference on Arabidopsis Research to be held June 22-25, 2011 in Madison, Wisconsin
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批准号:1118263
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财政年份:2011
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财政年份:2010
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依托单位:
The Arabidopsis SNI1 Complex Regulates Both Gene Transcription and DNA Recombination During the Defense Response
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财政年份:2008
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Arabidopsis 2010: Expression Profiling of Plant Disease Resistance Pathways
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财政年份:2005
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Chromsome Modification and Transcription Repression in Regulation of Systemic Acquired Resistance
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批准号:0445621
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项目类别:Continuing Grant
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资助金额:$48.0万
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财政年份:2005
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依托单位:
Arabidopsis 2010: Expression Profiling of Plant Disease Resistance Pathways
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依托单位:
Functional Analysis of NPR1 in SAR Signal Transduction
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资助金额:$36.7万
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财政年份:1998
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负责人:Xinnian Dong
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依托单位:
海外基金