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ISSN: 2329-9029

Journal of Plant Biochemistry & Physiology
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Research Article

Similarities and Differences in Global Gene Expression Profiles between Herbicide and Pathogen-Induced PSII Inhibition

Jin Zhu1, Min Li2 and Steven J Clough3,4*
1Monsanto, St. Louis, MO, USA
2Syngenta, Raleigh, NC, USA
3Department of Crop Sciences, University of Illinois, Urbana, IL 61801, USA
4United States Department of Agriculture- Agricultural Research Services, Urbana, IL 61801, USA
*Corresponding Author : Steven J. Clough
National Soybean Research Center
Department of Crop Sciences
University of Illinois, 1101 W.Peabody Drive
Urbana, IL 61801, USA
Tel: (217) 265-6452
E-mail: [email protected]
Received: September 30, 2015 Accepted: October 26, 2015 Published: November 02, 2015
Citation: Zhu J, Li M, Clough SJ (2015) Similarities and Differences in Global Gene Expression Profiles between Herbicide and Pathogen-Induced PSII Inhibition. J Plant Biochem Physiol 3:157. doi:10.4172/2329-9029.1000157
Copyright: © 2015 Zhu J, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Plant pathogens, and photosynthesis inhibiting herbicides, can both damage photosystem II (PSII), causing it to be highly sensitive to damage by light energy, and to release high levels of reactive oxygen species (ROS). This photoinhibition of PSII could possibly be the source of the strong oxidative burst associated with the pathogeninduced, hypersensitive defense response (HR). To examine a possible mechanism of how the HR-associated ROS burst could originate from PSII inhibition, we compared the transcriptome responses in soybean undergoing photoinhibition induced by HR, to soybean undergoing photoinhibition induced by the herbicide bentazon, which specially stops PSII electron flow by preventing QB from binding to D1. Most genes shared similar expression patterns between HR and bentazon treatments; however, interesting differences were also observed. The most striking differences were seen with genes related to photosynthesis, where these genes were uniformly down regulated in HR, but were mostly up in response to bentazon. Another interesting difference was seen in genes of the phenylpropanoid pathway. These defense-related genes were mostly down or non-responsive to bentazon, but were generally induced in response to pathogen-induced HR, showing that soybeans activate the phenylpropanoidbased phytoalexins independent of PSII inhibition. We conclude that the PSII inhibition occurring during the HR is not being triggered simply by the inhibition of electron flow through the photosystem centers. Instead, it is more likely that the initial triggers of the HR halt the repair of damaged PSII which leads to enhancing photoinhibition and contributing the rapid production of ROS, sealing the fate of cells undergoing HR; and the triggers independently induce specific aspects of defenses such as the phenylpropanoid pathway.

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