Secondary metabolite from NostocXPORK14A inhibits photosynthesis and growth of SynechocystisPCC 6803

Abstract

Screening of 55 different cyanobacterial strains revealed that an extract from NostocXPORK14A drastically modifies the amplitude and kinetics of chlorophyll a fluorescence induction of SynechocystisPCC 6803 cells. After 2d exposure to the NostocXPORK14A extract, SynechocystisPCC 6803 cells displayed reduced net photosynthetic activity and significantly modified electron transport properties of photosystem II under both light and dark conditions. However, the maximum oxidizable amount of P700 was not strongly affected. The extract also induced strong oxidative stress in SynechocystisPCC 6803 cells in both light and darkness. We identified the secondary metabolite of NostocXPORK14A causing these pronounced effects on Synechocystis cells. Mass spectrometry and nuclear magnetic resonance analyses revealed that this compound, designated as M22, has a non-peptide structure. We propose that M22 possesses a dual-action mechanism: firstly, by photogeneration of reactive oxygen species in the presence of light, which in turn affects the photosynthetic machinery of SynechocystisPCC 6803; and secondly, by altering the in vivo redox status of cells, possibly through inhibition of protein kinases. We identified the secondary metabolite of NostocXPORK14A causing these pronounced effects on SynechocystisPCC6803 cells by inhibiting photosynthesis and growth. This compound, designated as M22, has a non-peptide structure. We propose that M22 possesses a dual action mechanism: first, by photo-generation of reactive oxygen species in the presence of light, which in turn affects the photosynthetic machinery of SynechocystisPCC 6803; and second, by altering the in vivo redox status of cells, possibly through inhibition of protein kinases. © 2013 John Wiley & Sons Ltd.