Singlet oxygen (1O2) refers to the lowest excited electronic state of molecular oxygen. It easily oxidizes biological molecules and, therefore, is cytotoxic. In plant cells, 1O2 is formed mostly in the light in thylakoid membranes by reaction centers of photosystem II. In high concentrations, 1O2 destroys membranes, proteins and DNA, inhibits protein synthesis in chloroplasts leading to photoinhibition of photosynthesis, and can result in cell death. However, 1O2 also acts as a signal relaying information from chloroplasts to the nucleus, regulating expression of nuclear genes. In spite of its extremely short lifetime, 1O2 can diffuse from the chloroplasts into the cytoplasm and the apoplast. As shown by recent studies, 1O2-activated signaling pathways depend not only on the levels but also on the sites of 1O2 production in chloroplasts, and can activate two types of responses, either acclimation to high light or programmed cell death. 1O2 can be produced in high amounts also in root cells during drought stress. This review summarizes recent advances in research on mechanisms and sites of 1O2 generation in plants, on 1O2-activated pathways of retrograde- and cellular signaling, and on the methods to study 1O2 production in plants.

Phytotoxic macrolides attract attention as prototypes of new herbicides. However, their mechanisms of action (MOA) on plants have not yet been elucidated. This study addresses the effects of two ten-membered lactones, stagonolide A (STA) and herbarumin I (HBI) produced by the fungus Stagonospora cirsii, on Cirsium arvense, Arabidopsis thaliana and Allium cepa. Bioassay of STA and HBI on punctured leaf discs of C. arvense and A. thaliana was conducted at a concentration of 2 mg/mL to evaluate phenotypic responses, the content of pigments, electrolyte leakage from leaf discs, the level of reactive oxygen species, Hill reaction rate, and the relative rise in chlorophyll a fluorescence. The toxin treatments resulted in necrotic and bleached leaf lesions in the dark and in the light, respectively. In the light, HBI treatment caused the drop of carotenoids content in leaves on both plants. The electrolyte leakage caused by HBI was light-dependent, in contrast with that caused by STA. Both compounds induced light-independent peroxide generation in leaf cells but did not affect photosynthesis 6 h after treatment. STA (10 µg/mL) caused strong disorders in root cells of A. thaliana leading to the complete dissipation of the mitochondrial membrane potential one hour post treatment, as well as DNA fragmentation and disappearance of acidic vesicles in the division zone after 8 h; the effects of HBI (50 µg/mL) were much milder. Furthermore, STA was found to inhibit mitosis but did not affect the cytoskeleton in cells of root tips of A. cepa and C. arvense, respectively. Finally, STA was supposed to inhibit the intracellular vesicular traffic from the endoplasmic reticulum to the Golgi apparatus, thus interfering with mitosis. HBI is likely to have another main MOA, probably inhibiting the biosynthesis of carotenoids.

No abstract

No abstract

No abstract