జర్నల్ ఆఫ్ ప్లాంట్ బయోకెమిస్ట్రీ & ఫిజియాలజీ
అందరికి ప్రవేశం

నైరూప్య

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

Jin Zhu, David J Neece, Bernarda Calla and Steven J Clough

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.