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ARS Home » Midwest Area » Urbana, Illinois » Soybean/maize Germplasm, Pathology, and Genetics Research » Research » Publications at this Location » Publication #322417

Title: If photoinhibition of soybean photosystem II enhances the hypersensitive response, it is not solely due to blockage of electron transfer flow at D1

item ZHU, JIN - Monsanto Corporation
item Neece, David
item Calla, Bernarda
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., Neece, D.J., Calla Zalles, B., Clough, S.J. 2015. If photoinhibition of soybean photosystem II enhances the hypersensitive response, it is not solely due to blockage of electron transfer flow at D1. Journal of Plant Biochemistry & Physiology. 3:156. doi:10.4172/2329-9029.1000156.

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 determine the role of a specific protein, D1, within PSII. The D1 protein allows proper binding of molecules needed to allow electron transfer through PSII, and to thereby allow photosynthesis to happen. We used the herbicide bentazon that prevents D1 from binding to the molecules needed for electron transfer. Bentazon treatment did not enhance pathogen defense, which demonstrates that the blockage of electron transfer is not the main mechanism that plants use to enhance photoinhibition and increase defense to pathogens. An alternative explanation is that plants might instead prevent the removal of damaged D1 from PSII, and in this manner enhance photoinhibition, and production of pathogen defense chemicals. These results are of interested to those working to understand the mechanism by which plants resist pathogens.

Technical Abstract: 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.