Partial inhibition of ABA-induced stomatal closure by calcium-channel blockers.

ABA-induced increases in [Ca2+]cyt (cytosolic free Ca2+) may result from Ca2+ influx from the apoplast and/or release from intracellular stores. In this paper, Ca2+-channel blockers have been used to investigate this question in the detached epidermis of Commelina communis. Examples from the benzothiazepine, dihydropyridine and phenylalkylamine series all inhibited ABA-induced stomatal closure: (+/-) verapamil > nifedipine > diltiazem. Inhibition was partial, the magnitude of the effect being dependent on both the concentration of ABA and that of the channel blocker. The maximum inhibition observed in the presence of 100 nM ABA was approximately 66% at high (100 nM) concentrations of (+/-) verapamil or nifedipine. In the near absence of extracellular Ca2+ (2 mM EGTA) ABA-induced stomatal closure was reduced by approximately 22% and the inhibition by Ca2+-channel blockers abolished. Inhibition by (+/-) verapamil was totally reversible and exhibited signs of stereospecificity, the s(-) enantiomer being a more potent inhibitor of ABA-induced stomatal closure than the R(+) enantiomer. Bay K 8644 (a fluorinated analogue of nifedipine) exhibited biphasic action on 500 uM Ca2+-induced stomatal closure, i.e. agonistic at low concentrations (10 nM), antagonistic at high concentrations (> 10 nM to 100 uM), but did not affect ABA-induced stomatal closure. These results suggest that Ca2+ release from intracellular stores may be important in the ABA-induced increase in [Ca2+]cyt associated with stomatal closure. They do not, however, exclude a contribution of Ca2+ influx from the apoplast

Plant virus infections control stomatal development

Stomata are important regulators of carbon dioxide uptake and transpirational water loss. They also represent points of vulnerability as bacterial and fungal pathogens utilise this natural opening as an entry portal, and thus have an increasingly complex relationship. Unlike the situation with bacterial and fungal pathogens, we know very little about the role of stomata in viral infection. Here we report findings showing that viral infection influences stomatal development in two susceptible host systems (Nicotiana tabacum with TMV (Tobacco mosaic virus), and Arabidopsis thaliana with TVCV (Turnip vein-clearing virus)), but not in resistant host systems (Nicotiana glutinosa and Chenopodium quinoa with TMV). Virus infected plants had significantly lower stomatal indices in systemic leaves of susceptible systems; N. tabacum 9.8% reduction and A. thaliana 12.3% reduction, but not in the resistant hosts. Stomatal density in systemic leaves was also significantly reduced in virus infected A. thaliana by 19.6% but not in N. tabacum or the resistant systems. In addition, transpiration rate was significantly reduced in TMV infected N. tabacum

Divergent evolutionary trajectories of bryophytes and tracheophytes from a complex common ancestor of land plants

The origin of plants and their colonization of land fundamentally transformed the terrestrial environment. Here we elucidate the basis of this formative episode in Earth history through patterns of lineage, gene and genome evolution. We use new fossil calibrations, a relative clade age calibration (informed by horizontal gene transfer) and new phylogenomic methods for mapping gene family origins. Distinct rooting strategies resolve tracheophytes (vascular plants) and bryophytes (non-vascular plants) as monophyletic sister groups that diverged during the Cambrian, 515–494 million years ago. The embryophyte stem is characterized by a burst of gene innovation, while bryophytes subsequently experienced an equally dramatic episode of reductive genome evolution in which they lost genes associated with the elaboration of vasculature and the stomatal complex. Overall, our analyses reveal that extant tracheophytes and bryophytes are both highly derived from a more complex ancestral land plant. Understanding the origin of land plants requires tracing character evolution across a diversity of modern lineages

KIN7 kinase regulates the vacuolar TPK1 K+ channel during stomatal closure

Stomata are leaf pores that regulate CO 2 uptake and evapotranspirational water loss. By controlling CO 2 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 2-mediated stomatal closure. Second, we reveal that, during ABA- and CO 2-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 2-induced stomatal closure. Stomatal closure critically depends on K + release from the guard cell vacuole. Isner et al. show that the TPK1 vacuolar K + channel is important for ABA- and CO 2-mediated stomatal closure and that channel activation involves TPK1 phosphorylation by the KIN7 receptor-like protein kinase, which co-expresses in the tonoplast and plasma membrane