Calcium Signaling Preceding the Emission of Plant Volatiles in Plant–Insect Interactions

Abstract

Plants react to herbivore attack by activating elaborate defence mechanisms. The success of plants in withstanding herbivory depends on their ability to quickly recognize, decipher the incoming signal, and adequately respond to a wide array of attacking insects. In contrast to the somatic adaptive immune system of mammals involving mobile defender cells, plant immune responses rely on the ability of each cell to recognize and respond to herbivore attack and on systemic signals originating from infected or wounded sites. Plant Ca2+ signals are involved in a sizable array of intracellular signaling pathways after pest invasion. A Ca2+ signal is defined by the balanced activation of Ca2+ channels at different cellular membranes, which is followed by the subsequent inactivation of channels and activation of efflux transporters to terminate Ca2+ influx and to rebalance cellular Ca2+ homeostasis. Upon herbivore feeding, there is a dramatic Ca2+ influx, followed by the activation of Ca2+-dependent signal transduction pathways that include interacting downstream networks of kinases for defense responses. Like in animal cells, free intracellular Ca2+ ([Ca2+]cyt) variations in plant cells are key signals in many cellular regulatory functions, playing a major role in mediating various endogenous and exogenous signals. Ca2+-binding sensory proteins such as Ca2+-dependent protein kinases (CPKs) have been recently documented to mediate the signaling following Ca2+ influx after herbivory, in a phytohormone-independent manner. Here we review the sequence of signal transductions triggered by herbivory-invoked Ca2+ signaling leading to plant volatile emission by analyzing the connection between early events and the production of herbivore-induced volatile compounds.