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Antioxid Redox Signal. 2013 Jun 1;18(16):2145-62. doi: 10.1089/ars.2012.5124. Epub 2013 Mar 6.

Production, detection, and signaling of singlet oxygen in photosynthetic organisms.

Author information

1
Department of Environmental Toxicology, Eawag, Swiss Federal Institute of Aquatic Science and Technology, Dübendorf, Switzerland. anja.krieger-liszkay@cea.fr

Abstract

SIGNIFICANCE:

In photosynthetic organisms, excited chlorophylls (Chl) can stimulate the formation of singlet oxygen ((1)O(2)), a highly toxic molecule that acts in addition to its damaging nature as an important signaling molecule. Thus, due to this dual role of (1)O(2), its production and detoxification have to be strictly controlled.

RECENT ADVANCES:

Regulation of pigment synthesis is essential to control (1)O(2) production, and several components of the Chl synthesis and pigment insertion machineries to assemble and disassemble protein/pigment complexes have recently been identified. Once produced, (1)O(2) activates a signaling cascade from the chloroplast to the nucleus that can involve multiple mechanisms and stimulate a specific gene expression response. Further, (1)O(2) signaling was shown to interact with signal cascades of other reactive oxygen species, oxidized carotenoids, and lipid hydroperoxide-derived reactive electrophile species.

CRITICAL ISSUES:

Despite recent progresses, hardly anything is known about how and where the (1)O(2) signal is sensed and transmitted to the cytoplasm. One reason for that is the limitation of available detection methods challenging the reliable quantification and localization of (1)O(2) in plant cells. In addition, the process of Chl insertion into the reaction centers and antenna complexes is still unclear.

FUTURE DIRECTIONS:

Unraveling the mechanisms controlling (1)O(2) production and signaling would help clarifying the specific role of (1)O(2) in cellular stress responses. It would further enable to investigate the interaction and sensitivity to other abiotic and biotic stress signals and thus allow to better understand why some stressors activate an acclimation, while others provoke a programmed cell death response.

PMID:
23320833
DOI:
10.1089/ars.2012.5124
[Indexed for MEDLINE]

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