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Edinburgh, Scotland, United Kingdom - TAIR

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Post-translational modifications of the transcription<br />

co-activator NPR1 regulate plant<br />

immunity<br />

Systemic acquired resistance (SAR) is a plant immune response effective<br />

against a broad-spectrum of pathogens. Activation of SAR is associated with<br />

dramatic transcription reprogramming of over 2,200 genes to prioritize defense<br />

responses over normal cellular functions. The transcription co-activator NPR1<br />

directly or indirectly controls the expression of most of these genes. In the<br />

cytoplasm of resting cells, NPR1 forms an oligomer through redox-sensitive<br />

intermolecular disulfide bonds. Upon induction of SAR, changes in cellular redox<br />

result in the release of NPR1 monomers, which translocate to the nucleus and<br />

modulate gene transcription. To gain a better understanding of transcriptional<br />

regulation in SAR, we investigated pathogen-induced changes in the equilibrium<br />

between NPR1 oligomer/monomer conformations and studied the behavior of<br />

NPR1 in the nucleus. We found that distinct post-translational modifications of<br />

NPR1 control its activity. In the cytoplasm, S-nitrosylation of NPR1, a process in<br />

which nitric oxide is covalently attached to a cysteine thiol, promotes oligomer<br />

formation, while thioredoxins (TRX) facilitate the opposite oligomer-to-monomer<br />

reaction. Moreover, in the nucleus NPR1 activity is regulated by cycles of sitespecific<br />

phosphorylation coupled to ubiquitin-mediated degradation by the<br />

proteasome. Degradation not only restricted the activity of NPR1 in the absence<br />

of pathogen threat, it surprisingly also played a critical role in promoting coactivator<br />

activity upon induction of SAR. The intimate interplay between different<br />

post-translational modifications and their dynamic effects on NPR1 activity will<br />

be fundamental to our discussion of regulatory mechanisms that govern plant<br />

immune responses.<br />

78<br />

C27<br />

Thursday 15:15 - 15:30<br />

Plant Defence<br />

Steven Spoel1<br />

Yasuomi Tada2<br />

Zhonglin Mou3<br />

Natalie Spivey4<br />

Xinnian Dong4<br />

1Biology Department<br />

Duke University<br />

USA<br />

(Present address: Institute<br />

for Molecular Plant Science<br />

University of <strong>Edinburgh</strong><br />

UK)<br />

2Biology Department<br />

Duke University<br />

USA<br />

(Present address:<br />

Life Science Research<br />

Center<br />

Kagawa University<br />

Japan)<br />

3Department of<br />

Microbiology and Cell<br />

Science<br />

University of Florida<br />

USA<br />

4Biology Department<br />

Duke University<br />

USA

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