The role of Ca2+ conducting cyclic nucleotide gated ion channels in signal transduction cascades related to plant growth, development, pathogen defense and programmed cell death

Date of Completion

January 2008


Biology, Molecular|Agriculture, Plant Pathology|Biology, Plant Physiology




cAMP is known to act as a secondary messenger in plants; however no specific protein has been heretofore identified as activated by cAMP in a manner associated with a signaling cascade in plants. Ca 2+ influx has long been known as an early signal initiating cytosolic innate immune responses to pathogen perception in plant cells, but other molecular components linking pathogen recognition to Ca2+ influx are not delineated. We have recently identified a cyclic nucleotide gated channel (CNGC) gene product as facilitating the Ca2+ flux that initiates innate immune signaling in the plant cell cytosol; cyclic nucleotides activate conductance through this channel. Work undertaken as one part of the dissertation research reported here shows that elevation of cytosolic cAMP is a key event in this signaling cascade. We also show that CNGC2 can conduct Ca2+ into cells and provide a model linking the Ca2+ current to downstream NO production. However, the mechanism linking cytosolic Ca 2+ rise to NO generation during pathogen response signaling in plants is still unclear. Research described here suggests that the initial pathogen recognition signal of Ca2+ influx into the cytosol activates calmodulin (CaM) and/or a CaM-like protein (CML), which then acts to induce downstream NO synthesis (by activation of nitric oxide synthase (NOS)) as intermediary steps in a pathogen perception signaling cascade, leading to innate immune responses, including hypersensitive response (HR).^ Currently, little is known about the roles of CNGCs in plant growth and development. Here, we present evidence that primary roots of cngc1 loss-of-function mutant seedlings grew faster than roots of wild type (WT) plants and had larger angles of gravicurvature and less NO generation upon gravistimulation. These phenotypes could be due to disruption of channels formed (at least in part) by AtCNGC1, which contributes to Ca2+ uptake into plants (including roots) and alteration in Arabidopsis primary root growth. In another study, leaf Ca2+ accumulation is reduced in the leaves of cngc2 loss-of-function mutant ( dnd1) compared to WT. Many early senescence-associated phenotypes were more prominent in dnd1 leaves than WT. Application of an NO donor effectively rescues many dnd1 senescence related phenotypes. ^