THE GENERATION OF Ca²⁺ SIGNALS IN PLANTS

Abstract

The calcium ion is firmly established as a ubiquitous intracellular second messenger in plants. At their simplest, Ca(2+)-based signaling systems are composed of a receptor, a system for generating the increase in [Ca(2+)]cyt, downstream components that are capable of reacting to the increase in [Ca(2+)]cyt, and other cellular systems responsible for returning [Ca(2+)]cyt to its prestimulus level. Here we review the various mechanisms responsible for generating the stimulus-induced increases in [Ca(2+)]cyt known as Ca(2+) signals. We focus particularly on the mechanisms responsible for generating [Ca(2+)]cyt oscillations and transients and use Nod Factor signaling in legume root hairs and stimulus-response coupling in guard cells to assess the physiological significance of these classes of Ca(2+) signals.

Tonoplast calcium sensors CBL2 and CBL3 control plant growth and ion homeostasis through regulating V-ATPase activity in Arabidopsis

“…The H + transport activity of VATPase was measured as a quenching of the pH-sensitive fluorescent probe quinacrine. Proton translocation was initiated in purified tonoplast vesicles (100 µg) by rapid addition of 1 mL reaction buffer containing 10 mM Tris-Mes (pH 8.0), 250 mM mannitol, 6 mM MgSO 4 , 50 mM (CH 3 ) 4 NCl, 3 mM ATP and 3 µM quinacrine. Fluorescence quenching was monitored in a thermostated cell at 25 °C using a fluorescence spectrometer (Hitachi F-2700) at 427 nm excitation wavelength and 495 nm emission wavelength.…”

“…The Ca 2+ -dependent signaling pathways participate in many aspects of plant development and environmental responses [1][2][3]. It is generally believed that stimulus-specific calcium signals are encoded by temporally and spatially defined patterns of Ca 2+ fluctuations that result from concerted action of Ca 2+ transporters [4][5]. To decode these cellular "Ca 2+ signatures", plant cells are equipped with a variety of calcium sensor proteins, which undergo conformational changes upon Ca 2+ binding and regulate their target proteins that further orchestrate downstream responses [2,[6][7][8][9].…”

Roles of ion channels and transporters in guard cell signal transduction

“…Upon elevation of Ca 2þ cyt , inward K + channels are inhibited and S-and R-type anion channels are activated. A detailed discussion of roles for cytosolic Ca 2+ in initiation and maintenance of stomatal closure is beyond the focus of this review, but is available elsewhere [119,120]. It is certain that that PM Ca 2+ -channels are important players in regulation of GC Ca 2þ cyt status, and these channels are regulated by many of the same proteins and metabolites involved in GC ABA response.…”

“…However, whether a voltage-dependent shift of SV channel activity leads to Ca 2+ efflux in guard cells under physiological conditions is currently under debate [105,[149][150][151]. The release of Ca 2+ from the vacuole additionally involves several kinds of Ca 2+ -permeable channels that have been implicated by physiological experiments but not yet characterized at the molecular level, including InsP 3 -and InsP 6 -and cADPR-sensitive Ca 2+ -release channels [120].…”

Global Sensitivity Analysis of OnGuard Models Identifies Key Hubs for Transport Interaction in Stomatal Dynamics

“…Research at the cellular and molecular levels has focused on these inputs and their contributions to stomatal movements. A large body of work has highlighted Ca 2+ -independent and Ca 2+ -dependent signaling, the latter including elevations in free cytosolic Ca 2+ concentration ([Ca 2+ ] i ), protein kinase and phosphatase activities, which inactivate inward-rectifying K + channels and activate Cl 2 (anion) channels, as well as the changes in cytosolic pH that promote the outwardrectifying K + channels and solute loss (Keller et al, 1989;Blatt et al, 1990;Thiel et al, 1992;Lemtiri-Chlieh and MacRobbie, 1994;Blatt, 1998, 1999;for review, see Blatt, 2000;Hetherington and Brownlee, 2004;Kim et al, 2010;Lawson and Blatt, 2014;Jezek and Blatt, 2017).…”