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Plants activate a myriad of signaling cascades to tailor adaptive responses under environmental stresses, such as salinity. While the roles of exogenous karrikins (KARs) in salt stress mitigation are well comprehended, genetic evidence of KAR signaling during salinity responses in plants remains unresolved. Here, we explore the functions of the possible KAR receptor KARRIKIN-INSENSITIVE2 (KAI2) in Arabidopsis thaliana tolerance to salt stress by investigating comparative responses of wild-type (WT) and kai2 -mutant plants under a gradient of NaCl. Defects in KAI2 functions resulted in delayed and inhibited cotyledon opening in kai2 seeds compared with WT seeds, suggesting that KAI2 played an important role in enhancing seed germination under salinity. Salt-stressed kai2 plants displayed more phenotypic aberrations, biomass reduction, water loss and oxidative damage than WT plants. kai2 shoots accumulated significantly more Na+ and thus had a lower K+/Na+ ratio, than WT, indicating severe ion toxicity in salt-stressed kai2 plants. Accordingly, kai2 plants displayed a lower expression of genes associated with Na+ homeostasis, such as SALT OVERLY SENSITIVE (SOS) 1, SOS2, HIGH-AFFINITY POTASSIUM TRANSPORTER 1;1 (HKT1;1) and CATION–HYDROGEN EXCHANGER 1 (NHX1) than WT plants. WT plants maintained a better glutathione level, glutathione-related redox status and antioxidant enzyme activities relative to kai2 plants, implying KAI2's function in oxidative stress mitigation in response to salinity. kai2 shoots had lower expression levels of genes involved in the biosynthesis of strigolactones (SLs), salicylic acid and jasmonic acid and the signaling of abscisic acid and SLs than those of WT plants, indicating interactive functions of KAI2 signaling with other hormone signaling in modulating plant responses to salinity. Collectively, these results underpin the likely roles of KAI2 in the alleviation of salinity effects in plants by regulating several physiological and biochemical mechanisms involved in ionic and osmotic balance, oxidative stress tolerance and hormonal crosstalk. [ABSTRACT FROM AUTHOR]

One of the major constraints facing the large-scale production of cassava (Manihot esculenta) roots is the rapid postharvest physiological deterioration (PPD) that occurs within 72 h following harvest. One of the earliest recognized biochemical events during the initiation of PPD is a rapid burst of reactive oxygen species (ROS) accumulation. We have investigated the source of this oxidative burst to identify possible strategies to limit its extent and to extend cassava root shelf life. We provide evidence for a causal link between cyanogenesis and the onset of the oxidative burst that triggers PPD. By measuring ROS accumulation in transgenic low-cyanogen plants with and without cyanide complementation, we show that PPD is cyanide dependent, presumably resulting from a cyanide-dependent inhibition of respiration. To reduce cyanide-dependent ROS production in cassava root mitochondria, we generated transgenic plants expressing a codon-optimized Arabidopsis (Arabidopsis thaliana) mitochondrial alternative oxidase gene (AOX1A). Unlike cytochrome c oxidase, AOX is cyanide insensitive. Transgenic plants overexpressing AOX exhibited over a 10-fold reduction in ROS accumulation compared with wild-type plants. The reduction in ROS accumulation was associated with a delayed onset of PPD by 14 to 21 d after harvest of greenhouse-grown plants. The delay in PPD in transgenic plants was also observed under field conditions, but with a root biomass yield loss in the highest AOX-expressing lines. These data reveal a mechanism for PPD in cassava based on cyanideinduced oxidative stress as well as PPD control strategies involving inhibition of ROS production or its sequestration. [ABSTRACT FROM AUTHOR]

One of the major constraints facing the large-scale production of cassava (Manihot esculenta) roots is the rapid postharvest physiological deterioration (PPD) that occurs within 72 h following harvest. One of the earliest recognized biochemical events during the initiation of PPD is a rapid burst of reactive oxygen species (ROS) accumulation. We have investigated the source of this oxidative burst to identify possible strategies to limit its extent and to extend cassava root shelf life. We provide evidence for a causal link between cyanogenesis and the onset of the oxidative burst that triggers PPD. By measuring ROS accumulation in transgenic low-cyanogen plants with and without cyanide complementation, we show that PPD is cyanide dependent, presumably resulting from a cyanide-dependent inhibition of respiration. To reduce cyanide-dependent ROS production in cassava root mitochondria, we generated transgenic plants expressing a codon-optimized Arabidopsis (Arabidopsis thaliana) mitochondrial alternative oxidase gene (AOX1A). Unlike cytochrome c oxidase, AOX is cyanide insensitive. Transgenic plants overexpressing AOX exhibited over a 10-fold reduction in ROS accumulation compared with wild-type plants. The reduction in ROS accumulation was associated with a delayed onset of PPD by 14 to 21 d after harvest of greenhouse-grown plants. The delay in PPD in transgenic plants was also observed under field conditions, but with a root biomass yield loss in the highest AOX-expressing lines. These data reveal a mechanism for PPD in cassava based on cyanideinduced oxidative stress as well as PPD control strategies involving inhibition of ROS production or its sequestration. [ABSTRACT FROM AUTHOR]

Thiamin and thiamin pyrophosphate (TPP) are well known for their important roles in human nutrition and enzyme catalysis. In this work, we present new evidence for an additional role of these compounds in the protection of cells against oxidative damage. Arabidopsis (Arabidopsis thaliana) plants subjected to abiotic stress conditions, such as high light, cold, osmotic, salinity, and oxidative treatments, accumulated thiamin and TPP. Moreover, the accumulation of these compounds in plants subjected to oxidative stress was accompanied by enhanced expression of transcripts encoding thiamin biosynthetic enzymes. When supplemented with exogenous thiamin, wild-type plants displayed enhanced tolerance to oxidative stress induced by paraquat. Thiamin application was also found to protect the reactive oxygen species-sensitive ascorbate peroxidasel mutant from oxidative stress. Thiamin-induced tolerance to oxidative stress was accompanied by decreased production of reactive oxygen species in plants, as evidenced from decreased protein carbonylation and hydrogen peroxide accumulation. Because thiamin could protect the saucylic acid induction-deficient1 mutant against oxidative stress, thiamin-induced oxidative protection is likely independent of salicylic acid signaling or accumulation. Taken together, our studies suggest that thiamin and TPP function as important stress-response molecules that alleviate oxidative stress during different abiotic stress conditions. [ABSTRACT FROM AUTHOR]

Reactive oxygen species play a critical role in mediating the oxidative damage that causes senescence in a variety of aerobic organisms, from yeast to mammals. Genetic studies of these organisms have revealed that extended longevity is frequently associated with an increased resistance to stress. However, the relationship between life span and oxidative stress tolerance in plants is poorly understood. We have investigated the responses to oxidative stress in the delayed leaf senescence mutants of Arabidopsis thaliana, ore1, ore3, and ore9. The detached leaves of these mutants exhibit increased tolerance to various types of oxidative stress. The ore1, ore3, and ore9 mutants were also more tolerant to oxidative stress at the level of the whole plant, as determined by measuring physiological and molecular changes associated with oxidative stress. However, the activities of antioxidant enzymes were similar or lower in the mutants, as compared to wild type. These results suggest that the increased resistance to oxidative stress in the ore1, ore3, and ore9 mutants is not due to enhanced activities of these antioxidant enzymes. Taken together, our findings provide genetic evidence that oxidative stress tolerance is linked to control of leaf longevity in plants. [ABSTRACT FROM AUTHOR]