Singlet Oxygen Inhibits the Repair of Photosystem II by Suppressing the Translation Elongation of the D1 Protein in Synechocystis sp. PCC 6803

Singlet oxygen, generated during photosynthesis, is a strong oxidant that can, potentially, damage various molecules of biological importance. We investigated the effects in vivo of singlet oxygen on the photodamage to photosystem II (PSII) in the cyanobacterium Synechocystis sp. PCC 6803. Increases...

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Published inBiochemistry (Easton) Vol. 43; no. 35; pp. 11321 - 11330
Main Authors Nishiyama, Yoshitaka, Allakhverdiev, Suleyman I., Yamamoto, Hiroshi, Hayashi, Hidenori, Murata, Norio
Format Journal Article
LanguageEnglish
Published United States American Chemical Society 07.09.2004
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Summary:Singlet oxygen, generated during photosynthesis, is a strong oxidant that can, potentially, damage various molecules of biological importance. We investigated the effects in vivo of singlet oxygen on the photodamage to photosystem II (PSII) in the cyanobacterium Synechocystis sp. PCC 6803. Increases in intracellular concentrations of singlet oxygen, caused by the presence of photosensitizers, such as rose bengal and ethyl eosin, stimulated the apparent photodamage to PSII. However, actual photodamage to PSII, as assessed in the presence of chloramphenicol, was unaffected by the production of singlet oxygen. These observations suggest that singlet oxygen produced by added photosensitizers acts by inhibiting the repair of photodamaged PSII. Labeling of proteins in vivo revealed that singlet oxygen inhibited the synthesis of proteins de novo and, in particular, the synthesis of the D1 protein. Northern blotting analysis indicated that the accumulation of psbA mRNAs, which encode the D1 protein, was unaffected by the production of singlet oxygen. Subcellular localization of polysomes with bound psbA mRNAs suggested that the primary target of singlet oxygen might be the elongation step of translation.
Bibliography:istex:3DCAA2A671B23FD673EC2A4E695479249E9BE8B2
This work was supported in part by Grants-in-Aid for Scientific Research (14740441 and 15013243 to Y.N. and 13854002 to N.M.) from the Ministry of Education, Culture, Sports, Science, and Technology of Japan. This work was also supported in part by the Cooperative Research Program of the National Institute for Basic Biology.
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ISSN:0006-2960
1520-4995
DOI:10.1021/bi036178q