Abstract
The modulation of guard cell function is the basis of stomatal closure, essential for optimizing water use and CO2 uptake by leaves. Nitric oxide (NO) in guard cells plays a very important role as a secondary messenger during stomatal closure induced by effectors, including hormones. For example, exposure to abscisic acid (ABA) triggers a marked increase in NO of guard cells, well before stomatal closure. In guard cells of multiple species, like Arabidopsis, Vicia and pea, exposure to ABA or methyl jasmonate or even microbial elicitors (e.g., chitosan) induces production of NO as well as reactive oxygen species (ROS). The role of NO in stomatal closure has been confirmed by using NO donors (e.g., SNP) and NO scavengers (like cPTIO) and inhibitors of NOS (L-NAME) or NR (tungstate). Two enzymes: a L-NAME-sensitive, nitric oxide synthase (NOS)-like enzyme and a tungstate-sensitive nitrate reductase (NR), can mediate ABA-induced NO rise in guard cells. However, the existence of true NOS in plant tissues and its role in guard cell NO-production are still a matter of intense debate. Guard cell signal transduction leading to stomatal closure involves the participation of several components, besides NO, such as cytosolic pH, ROS, free Ca2+, and phospholipids. Use of fluorescent dyes has revealed that the rise in NO of guard cells occurs after the increase in cytoplasmic pH and ROS. The rise in NO causes an elevation in cytosolic free Ca2+ and promotes the efflux of cations as well as anions from guard cells. Stomatal guard cells have become a model system to study the signaling cascade mechanisms in plants, particularly with NO as a dominant component. The interrelationships and interactions of NO with cytosolic pH, ROS, and free Ca2+ are quite complex and need further detailed examination. While assessing critically the available literature, the present review projects possible areas of further work related to NO-action in stomatal guard cells.
Highlights
Stomatal pores are the gateways for transpirational H2O loss and entry of carbon dioxide (CO2) into leaves
CONCLUDING REMARKS The available literature amply demonstrates that Nitric oxide (NO) is a common signaling component and a converging step for events initiated by abscisic acid (ABA), methyl jasmonate (MJ), or elicitors
The upstream components of NO, which rise during ABA action, are broadly understood
Summary
Stomatal pores are the gateways for transpirational H2O loss and entry of CO2 into leaves. Due to such dual role, the regulation of stomatal aperture, and yet maintenance of opening are essential to keep up the water balance and at the same. Some of the plant hormones (ABA, MJ, ethylene), salicylic acid, polyamines and even elicitors (mostly microbial) cause stomatal closure, while auxins and cytokinins promote stomatal opening (Bright et al, 2006; Acharya and Assmann, 2009; Alcázar et al, 2010; Jing et al, 2012; Ye et al, 2013). The rise in NO of guard cells is a common and dominant event during stomatal closure induced by several effectors and in different plants (Table 1)
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