|Sang Gu, Kang|
|Natarajan, Savithiry - Savi|
Submitted to: Proteomics
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 4/8/2007
Publication Date: 7/5/2007
Citation: Sang Gu, K., Nurul, M., Bae, H., Natarajan, S.S. 2007. Proteome Analysis and Characterization of Phenotypes of Lesion Mimic Mutant Spotted Leaf 6 in Rice. Proteomics(2007). 7:2447-2458 Interpretive Summary: The rice mutant, spotted leaf 6 (spl6), shows necrotic spots as it matures without any disease. As it matures, small scattered reddish brown spots develop naturally on the leaves. We compared the total leaf proteins of the normal and the spl6 rice. The proteins from mutant leaves showed a reduced level of many beneficial proteins that are important for the protection of the plant. By understanding the mechanism of how these spots develop, it is possible to improve the resistance of rice plants, which will benefit farmers and the rice industries through increased yields.
Technical Abstract: Rice spotted leaf 6 (spl6) creates spontaneous cell death in the absence of pathogenic infection. In plant maturation stage, small reddish brown and scattered spots were arranged in groups and were made longitudinal parallel line along the midrib on the leaf blade, indicating that the expression of this genetic trait is developmentally programmed. Under light microscopy and transmission electron microscopy, damaging thylakoid membranes in chloroplasts of mesophyll cells were clearly observed in the nonspotted leaf section of the mutant. However, chloroplasts were not observed in the mesophyll cells of spotted area of spl6 mutant. These results indicated that spot formation of spl6 mutant may be caused by oxidative burst. About 159 protein spots were found to be up- and down-regulated in comparison between normal leaves of wild type and spotted leaves of spl6 mutant. Among them, we found protein disulfide isomerase (PDI), transketolase (TK), thioredoxin peroxidase (TPX), ATP synthase, phytochrome, rubisco large subunit and rubisco activase small subunit were not expressed in spl6 mutant but abundant in wild type. Absence of TPX and PDI may possibly fail to protect cells against oxidative burst resulting in degradation of thylakoid membranes and leading to programmed cell death. This may induce developmentally programmed lesion formation in the spl6 mutant. Overall results of this study suggest that malfunction of the spl6 gene in the rice spl6 mutant may result in degradation of chloroplast structure by oxidative burst.