Figure 1.

Signal crosstalk during NO-regulated stomatal closure in turgid leaves of Arabidopsis thaliana. In turgid leaves ABA-induced stomatal closure is dependent on the synthesis of H₂O₂ by various NADPH oxidases and the subsequent synthesis of nitric oxide (NO) by nitrate reductase 1 (NR1).¹⁶ NO signals via a Ca²⁺-dependent ABA signaling pathway,⁴ possibly by the S-nitrosylation of Ca²⁺-dependent ion channels.¹⁵ Numerous environmental signals modulate this response and determine the actual stomatal apertures observed.⁴,¹⁹ Interestingly the ABA-induced accumulation of H₂O₂ in turgid guard cells also appears to depend on the ability of the ethylene receptor, ETR1, to perceive ethylene and although not actually required for the ABA-induced accumulation of this reactive oxygen species, downstream components of the ethylene signal transduction pathway also seem to be required for H₂O₂ to signal its presence in these cells.¹⁷,²¹ Thus, the synthesis and signaling of H₂O₂ and NO in turgid guard cells may constitute points of convergence of ABA and ethylene signaling. However, numerous question remain concerning how the activities of the NADPH oxidases and NR1 are regulated and whether or not this occurs via the direct regulation of the extant proteins or via increased transcription as a result of ABA and ethylene signaling. Additionally, questions remain as to exactly how H₂O₂ induces NR1-mediated NO synthesis and whether this is either by the direct modulation of protein activity or as a result of downstream signaling. For example, H₂O₂ may signal in its own right or may mediate the activity of components of the ethylene signal transduction chain leading to an increase in NIA1 transcription. Future studies aim to clarify these questions.