Nitric oxide triggers specific and dose-dependent cytosolic calcium transients in Arabidopsis

Abstract

Equally, plants possess signal transduction networks that are highly conserved in terms of components which are also as sophisticated as that in their mammalian counterparts. 2 In the resting (un-stimulated) state, the cytosolic free Ca 2+ concentration [Ca 2+ ] cyt is ~200 nM and most of the cellular calcium is sequestered in cytoplasmic organelles such as the vacuole (100 mM), endoplasmic reticulum (ER) (1 mM), or the cell wall (1 mM). 3 This difference of many orders of magnitude in free Ca 2+ concentrations between the cytoplasm and cytosolic compartments creates a large electrochemical Ca 2+ gradient (200-300 mV), across the plasma membrane (PM), ER, and tonoplast that favours the energy-independent (downhill) movement of Ca 2+ into the cytosol (influx). This movement is controlled by a diverse set of specialized Ca 2+ channels and pores. Conversely, the movement of Ca 2+ against this electrochemical gradient, from the cytoplasm into the stores (efflux), is energy-dependent, and, requires ATP or proton motive force and is provided by specialized Ca 2+ -ATPase pumps. Both types of proteins, channels and pumps, are abundant in the PM and tonoplast and also occur in the ER, mitochondria and chloroplasts. 3,4 The channels that are responsible for Ca 2+ influx into the cytosol are gated by either voltage, stretch, inositol triphosphate (IP3), cADPR or G-proteins. Ca 2+ -mediated signaling takes place when some of these channels open, allowing Ca 2+ to move down the electrochemical gradient. 4 2+ or Ca 2+ fluxes function in many biochemical and processes including: red light, abscisic acid, gibberellin, salinity/drought, hypo-osmotic stress, touch, cold, heat shock, and nodulation factors. 6-8 Moreover, Ca 2+ fluxes play a pivotal role in developmental and physiological processes such as: egg cell fertilisation, 9 pollen tube elongation, 10 circadian rhythms, 11 oxidative stress 12,13 and pathogen infection. 14 The ability of a plant cell to differentiate among various Ca 2+ signals to activate the correct set of cellular responses is intriguing. Each signal creates its own Ca 2+ fingerprint that is unique in the lag period, frequency and amplitude of the Ca 2+ wave, and its spatial distribution. The targets of Ca 2+ signal transduction can be divided into two categories: primary sensors and downstream substrates. Phosphorylation cascades regulated by protein kinases [Plant Signaling & Behavior 4:3, 191-196; March 2009]

Nitric oxide-activated calcium/calmodulin-dependent protein kinase regulates the abscisic acid-induced antioxidant defence in maize

“…It has been reported that NO is involved in the ABA-induced antioxidant defence system and NO functions both upstream and downstream of Ca 2+ /CaM in plants ( Zhang et al ., 2007 ; Sang et al ., 2008 ; Aboul-Soud et al ., 2009 ). To establish a link between NO and ZmCCaMK in ABA signalling, the NO donor SNP was used.…”

Regulation of the Fruit-Specific PEP Carboxylase SlPPC2 Promoter at Early Stages of Tomato Fruit Development

“…In addition, several motifs identified as binding sites for transcription factors (MADS domain factors, TCP, WRKY) were also found upstream of transcription start ( Figure 1 ). Of particular interest is the −1500 to −900 region where motifs putatively involved in the binding of MADS domain protein (CArG box) [44] and in signalling pathways for auxin and brassinosteroid (ARFAT) [45] , gibberellin (GADOWNAT and GARE) [46] , [47] , abscisic acid and calcium (ABRE-like motif) [48] , [49] and ethylene (ERE) [50] were found. In plants, regulatory elements usually tend to be highly clustered in the vicinity of the core-promoter elements, but can also be found all along the promoter [51] , [52] .…”

Molecular mechanisms governing plant responses to high temperatures

“…In animal cells, NO functions as a secondary messenger to mobilize Ca 2+ from intracellular stores (Galione ). NO can increase [Ca 2+ ] in tobacco and Arabidopsis , and this increase in Ca 2+ can be inhibited by a pretreatment with c‐PTIO, suggesting that the induction is specifically mediated by NO (Lamotte et al ; Aboul‐Soud et al ). This NO‐induced accumulation of Ca 2+ can be significantly blocked by inhibitors of the Ca 2+ channels in the membrane, including La 3+ and Gd 3+ , and less significantly blocked by the intracellular Ca 2+ channel inhibitor 8‐bromo cADPR.…”

“…This NO‐induced accumulation of Ca 2+ can be significantly blocked by inhibitors of the Ca 2+ channels in the membrane, including La 3+ and Gd 3+ , and less significantly blocked by the intracellular Ca 2+ channel inhibitor 8‐bromo cADPR. This suggests that the plasma membrane channel‐mediated influx of Ca 2+ is the main contributor to the NO‐induced elevation in cellular Ca 2+ (Lamotte et al ; Aboul‐Soud et al ). Considering the time it takes for heat exposure to induce the accumulation of intracellular Ca 2+ and NO, it is reasonable to conclude that NO acts downstream of Ca 2+ in the regulation of plant HS signaling, suggesting that NO feedback could enhance the Ca 2+ ‐mediated HS signaling, via an unknown mechanism.…”