Plant pathogen attacks are perceived through pathogen-issued compounds or plant-derived molecules that elicit defense reactions. Despite the large variety of elicitors, general schemes for cellular elicitor signaling leading to plant resistance can be drawn. In this article, we review early signaling events that happen after elicitor perception, including reversible protein phosphorylations, changes in the activities of plasma membrane proteins, variations in free calcium concentrations in cytosol and nucleus, and production of nitric oxide and active oxygen species. These events occur within the first minutes to a few hours after elicitor perception. One specific elicitor transduction pathway can use a combination or a partial combination of such events which can differ in kinetics and intensity depending on the stimulus. The links between the signaling events allow amplification of the signal transduction and ensure specificity to get appropriate plant defense reactions. This review first describes the early events induced by cryptogein, an elicitor of tobacco defense reactions, in order to give a general scheme for signal transduction that will be use as a thread to review signaling events monitored in different elicitor or plant models.

are natural counterparts in vascular function, and it is becoming increasingly clear that an imbalance between these two mediators is a characteristic of endothelial dysfunction and is important in the progression of vascular disease. Here, we review classical and more recent data that suggest that ET-1 should be regarded as an essential component of NO signaling. In particular, we review evidence of the role of ET-1 in models of acute and chronic NO synthase blockade. Furthermore, we discuss the possible mechanisms by which NO modulates ET-1 activity. On the basis of these studies, we suggest that NO tonically inhibits ET-1 function, and in conditions of diminished NO bioavailability, the deleterious effects of unmitigated ET-1 actions result in vasoconstriction and eventually lead to vascular remodeling and dysfunction.ONCE THOUGHT TO BE AN INERT barrier delineating the boundaries of the circulation, the endothelium is now known to be a critical junction of vascular signaling. The endothelium produces and is acted upon by a host of mediators in what appears to be an exceedingly complex and interrelated signalome. With its capacity to release mediators involved in vasoconstriction, vasodilation, cell adhesion, growth, differentiation, proliferation, and motility, normal endothelial function is a prerequisite for cardiovascular health. Indeed, endothelial dysfunction, characterized by altered production of vasoactive substances, often precedes the overt manifestation of disease and is considered an important etiological factor in the progression of cardiovascular diseases.Endothelin-1 (ET-1) has been known to be an important mediator of vascular function since its discovery by Yanagisawa et al. in the late 1980's (106). Due to its potent and long-lasting vasoconstrictor effects, its capacity to induce vascular remodeling, fibrosis, cell proliferation, apoptosis, and its link to oxidative stress, ET-1 has been proposed to be important in the progression of numerous pathologies (51). The recognition of its importance in cardiovascular disease is perhaps best illustrated by the observation of Barton and Yanagisawa that within 4 years of ET-1's discovery, its receptors had been cloned and pharmacological antagonists had been developed; these therapeutics were being tested in clinical trials by the early 1990's (8). However, despite intensive study over the past two decades and the relative success of ET-1 antagonists in certain conditions [e.g., pulmonary hypertension (71), congestive heart failure (83)], the precise role of ET-1 in vascular physiology and pathophysiology has stubbornly eluded investigators. This may be due, in part, to several intricacies of the ET-1 system that makes it inherently complex [e.g., receptor localization, receptor dimerization (100)].Notwithstanding these difficulties, ET-1, like many vascular mediators, is an intrinsically complicated system by virtue of the fact that its function in physiology and pathophysiology is inextricably linked with other vascular mediators, most notably nit...

No abstract