Salinity is a major threat to modern agriculture causing inhibition and impairment of crop growth and development. Here, we not only review recent advances in salinity stress research in plants but also revisit some basic perennial questions that still remain unanswered. In this review, we analyze the physiological, biochemical, and molecular aspects of Na + and Cl − uptake, sequestration, and transport associated with salinity. We discuss the role and importance of symplastic versus apoplastic pathways for ion uptake and critically evaluate the role of different types of membrane transporters in Na + and Cl − uptake and intercellular and intracellular ion distribution. Our incomplete knowledge regarding possible mechanisms of salinity sensing by plants is evaluated. Furthermore, a critical evaluation of the mechanisms of ion toxicity leads us to believe that, in contrast to currently held ideas, toxicity only plays a minor role in the cytosol and may be more prevalent in the vacuole. Lastly, the multiple roles of K + in plant salinity stress are discussed.

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Stomata are leaf pores that regulate CO uptake and evapotranspirational water loss. By controlling CO uptake, stomata impact on photosynthesis and dry matter accumulation. The regulation of evapotranspiration is equally important because it impacts on nutrient accumulation and leaf cooling and enables the plant to limit water loss during drought [1]. Our work centers on stomatal closure [2-6]. This involves loss of potassium from the guard cell by a two-step process. Salt is released across the plasma membrane via anion channels such as SLAC1 [7-9] and depolarization-activated channels such as GORK [10, 11], with the net result that cations and anions exit guard cells. However, this critically depends on K release from the vacuole; with ∼160 and 100 mM K in cytoplasm and vacuole of open guard cells [12], vacuolar K efflux is driven by the negative tonoplast potential, and this expels K from the vacuole via tonoplast K channels like TPK1. In all, guard cell salt release leads to a loss of turgor that brings about stomatal closure. First, we show that the TPK1 vacuolar K channel is important for abscisic acid (ABA)- and CO-mediated stomatal closure. Second, we reveal that, during ABA- and CO-mediated closure, TPK1 is phosphorylated and activated by the KIN7 receptor-like protein kinase (RLK), which co-expresses in the tonoplast and plasma membrane. The net result is K release from the vacuole. Taken together, our work reveals new components involved in guard cell signaling and describes a new mechanism potentially involved in fine-tuning ABA- and CO-induced stomatal closure.

Arsenic is toxic to all life forms and is a potent carcinogen. Its accumulation in crop plants and subsequent consumption poses a serious threat to public health worldwide. Recent developments have enhanced our understanding of the molecular mechanisms governing arsenic uptake, detoxification, and accumulation in plants. In particular, the identification of plant arsenate reductase enzymes and emerging details of the processes underlying arsenic distribution and deposition in the seed will prove invaluable in the development of new strategies to mitigate this threat. Here we provide an outline of these recent developments and suggest new molecular mechanisms that could be employed to reduce arsenic in crops.

All living organisms communicate with their environment, and part of this dialogue is mediated by secondary messengers such as cyclic guanosine mono phosphate (cGMP). In plants, most of the specific components that allow production and breakdown of cGMP have now been identified apart from cGMP dependent phosphodiesterases, enzymes responsible for cGMP catabolism. Irrespectively, the role of cGMP in plant signal transductions is now firmly established with involvement of this nucleotide in development, stress response, ion homeostasis and hormone function. Within these areas, several consistent themes where cGMP may be particularly relevant are slowly emerging: these include regulation of cation fluxes, for example via cyclic nucleotide gated channels and in stomatal functioning. Many details of signalling pathways that incorporate cGMP remain to be unveiled. These include downstream targets other than a small number of ion channels, in particular cGMP dependent kinases. Improved genomics tools may help in this respect, especially since many proteins involved in cGMP signalling appear to have multiple and often overlapping functional domains which hampers identification on the basis of simple homology searches. Another open question regards the topographical distribution of cGMP signals are they cell limited? Does long distance cGMP signalling occur and if so, by what mechanisms? The advent of non-disruptive fluorescent reporters with high spatial and temporal resolution will provide a tool to accelerate progress in all these areas. Automation can facilitate large scale screens of mutants or the action of effectors that impact on cGMP signalling.

Summary Although UVA radiation (315–400 nm) represents 95% of the UV radiation reaching the earth’s surface, surprisingly little is known about its effects on plants [ 1 ]. We show that in Arabidopsis , short-term exposure to UVA inhibits the opening of stomata, and this requires a reduction in the cytosolic level of cGMP. This process is independent of UVR8, the UVB receptor. A cGMP-activated phosphodiesterase ( AtCN-PDE1 ) was responsible for the UVA-induced decrease in cGMP in Arabidopsis . AtCN-PDE1-like proteins form a clade within the large HD-domain/PDEase-like protein superfamily, but no eukaryotic members of this subfamily have been functionally characterized. These genes have been lost from the genomes of metazoans but are otherwise conserved as single-copy genes across the tree of life. In longer-term experiments, UVA radiation increased growth and decreased water-use efficiency. These experiments revealed that PDE1 is also a negative regulator of growth. As the PDE1 gene is ancient and not represented in animal lineages, it is likely that at least one element of cGMP signaling in plants has evolved differently to the system present in metazoans.

Genome-wide association studies were used to analyse potassium use efficiency in rice. Novel associations were found along with a role for sodium replacement via the OsHKT2;1 sodium transporter.

High concentration of arsenic (As) in rice is a serious problem worldwide. Pot experiments were conducted to assess the potential dietary toxicity of arsenic and effect of various soil amendments on arsenic accumulation in rice grains. Two basmati rice genotypes were used to conduct pot experiments using various levels of arsenic (10, 25, 50 and 100 mg kg-1 soil). In addition, plants were exposed to soil collected from a well documented arsenic contaminated site. Contrasting results for growth, yield and grain arsenic concentration were obtained for basmati-385 (Bas-385), exhibiting tolerance (56% yield improvement at 10 mg As kg-1), while genotype BR-1 showed 18% yield decline under same conditions. Furthermore, application of soil amendments such as iron (Fe), phosphate (PO 4) and farmyard manure (FYM) at 50 mg kg-1 , 80 kg ha-1 and 10 t ha-1 , respectively improved the plant height and biomass in both genotypes. Accumulation of arsenic in rice grain followed a linear trend in BR-1 whereas a parabolic relationship was observed in Bas-385. Both genotypes exhibited a positive response to iron sulfate amendment with significant reduction in grain arsenic concentrations. Regression analysis gave soil arsenic threshold values of 12 mg kg-1 in Bas-385 and 10 mg kg-1 in BR-1 for potential dietary toxicity. This study suggests that genotype Bas-385 can be used for safe rice production in areas with soil arsenic contamination up to 12 mg kg-1 and that appropriate dose of iron sulfate for soil amendment can be used effectively to reduce translocation of arsenic to rice grain.