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ARS Home » Midwest Area » Urbana, Illinois » Soybean/maize Germplasm, Pathology, and Genetics Research » Research » Publications at this Location » Publication #322423

Title: Similarities and differences in global gene expression profiles between herbicide- and pathogen-induced PSII inhibition

item ZHU, JIN - Monsanto Corporation
item LI, MIN - Syngenta
item Clough, Steven

Submitted to: Journal of Plant Biochemistry & Physiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/26/2015
Publication Date: 11/2/2015
Citation: Zhu, J., Li, M., Clough, S.J. 2015. Similarities and differences in global gene expression profiles between herbicide- and pathogen-induced PSII inhibition. Journal of Plant Biochemistry & Physiology. 3:157. doi:10.4172/2329-9029.1000157.

Interpretive Summary: It has been proposed that plants could use the power of the sun to enhance defense to pathogens. Earlier work by our group and others showed that one of the photosystem centers, PSII, is inhibited during pathogen defense, and PSII inhibition is well documented to lead to rapid production of defense chemicals when stimulated by light. The objective of our research was to compare gene expression patterns in soybean in respone to a pathogen that induces photoinhibition, to gene expression patterns in soybean treated with an herbicide that induces photoinhibition. If the two treatments share the same mechanism for inhibiting PSII, than we should be able to see that in the gene expression responses. The results revealed that the two treatments are inducing photoinhibition by different mechanism, and that plant defense most likely involves a mechinism that is preventing the plants from reparing and replacing damaged PSII, and that this aids the defense response. These results are of interested to those working to understand the mechanism by which plants resist pathogens.

Technical 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 pathogen-induced, 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 phenylpropanoid-based 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.