Role of nitric oxide in regulating stomatal apertures

During stomatal closure, nitric oxide (NO) operates as one of the key intermediates in the complex, abscisic acid (ABA)-mediated, guard cell signaling network that regulates this process. However, data concerning the role of NO in stomatal closure that occurs in turgid vs. dehydrated plants is limited. The data presented demonstrate that, while there is a requirement for NO during the ABA-induced stomatal closure of turgid leaves, such a requirement does not exist for ABA-enhanced stomatal closure observed to occur during conditions of rapid dehydration. The data also indicate that the ABA signaling pathway must be both functional and to some degree activated for guard cell NO signaling to occur. These observations are in line with the idea that the effects of NO in guard cells are mediated via a Ca(2+)-dependent rather than a Ca(2+)-independent ABA signaling pathway. It appears that there is a role for NO in the fine tuning of the stomatal apertures of turgid leaves that occurs in response to fluctuations in the prevailing environment.