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ISSN: 2329-9029

Journal of Plant Biochemistry & Physiology
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Research Article

If Photoinhibition of Soybean Photosystem II Enhances the Hypersensitive Response, It is Not Solely Due to Blockage of Electron Transfer Flow at D1

Jin Zhu1, David J Neece2, Bernarda Calla1 and Steven J Clough1,2*
1Department of Crop Sciences, University of Illinois, Urbana, IL, USA
2Agricultural Research Services, United States Department of Agriculture, Urbana, IL, 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, Neece DJ, Calla B, Clough CJ (2015) If Photoinhibition of Soybean Photosystem II Enhances the Hypersensitive Response, It is Not Solely Due to Blockage of Electron Transfer Flow at D1. J Plant Biochem Physiol 3:156. doi:10.4172/2329-9029.1000156
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.
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Previous studies have suggested that photoinhibition, through inactivation of photosystem II (PSII), could be beneficial to plants during defense to pathogens through enhanced reactive oxygen (ROS), especially during the hypersensitive response (HR). In this study, we addressed this question by focusing on a possible role of turnover and inhibition of the PSII subunit D1, in defense to the compatible and incompatible strains of the bacterial pathogen Pseudomonas syringae in soybean leaves. Expression of the D1 encoding gene, psbA, as well as 14 other chloroplast encoded genes, was down regulated in response to P. syringae. This down regulation is consistent with reduced production of PSII components leading to increased photoinhibition of existing photocenters, and is also consistent with multiple studies showing a concerted down regulation of nuclear-encoded chloroplast genes during pathogen attack. However, although expression of the psbA transcript was reduced in response to pathogen within 8 hours of inoculation, the level of the psbA product, the D1 protein, showed no significant changes via western blots, and did not show any signs of degradation. Additionally, infiltrating leaves with the D1 inhibiting herbicide bentazon (competitive inhibitor of QB binding to D1, stopping photosynthesis by blocking electron transfer from QA to QB) together with P. syringae inoculation, showed that D1 inhibition did not enhance defense as expected (if photoinhibition enhanced defense), but actually rendered the host slightly more susceptible. The results reflect two possibilities. One is that PSII inhibition through blockage of electron flow through D1 of PSII, does not enhance resistance to P. syringae. The second possibility supported by the data is that the mechanism of photoinhibition during pathogen defense is not due solely to the blockage of electron flow, but through another means of stimulating photoinhibition, such as an inefficient degradation, removal, and replacement of damaged D1 from the PSII complex.


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