115 Phosphoinositide signal transduction in guard cells

1998 ◽  
Vol 26 (4) ◽  
pp. S397-S397
Author(s):  
Fiona L. Aitken ◽  
Christophe Pical ◽  
Bernd Müller-Röber ◽  
Joachim Kopka ◽  
Julie E. Gray
Keyword(s):  
Signal Transduction ◽  
Guard Cells

scholarly journals Abscisic acid-independent stomatal CO2 signal transduction pathway and convergence of CO2 and ABA signaling downstream of OST1 kinase

2018 ◽  
Vol 115 (42) ◽  
pp. E9971-E9980 ◽  
Author(s):  
Po-Kai Hsu ◽  
Yohei Takahashi ◽  
Shintaro Munemasa ◽  
Ebe Merilo ◽  
Kristiina Laanemets ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Abscisic Acid ◽  
Protein Kinase ◽  
Stomatal Closure ◽  
Signal Transduction Pathway ◽  
Guard Cells ◽  
Aba Signaling ◽  
Time Resolved ◽  
Aba Receptor ◽  
Biochemical Analyses

Stomatal pore apertures are narrowing globally due to the continuing rise in atmospheric [CO2]. CO2 elevation and the plant hormone abscisic acid (ABA) both induce rapid stomatal closure. However, the underlying signal transduction mechanisms for CO2/ABA interaction remain unclear. Two models have been considered: (i) CO2 elevation enhances ABA concentrations and/or early ABA signaling in guard cells to induce stomatal closure and (ii) CO2 signaling merges with ABA at OST1/SnRK2.6 protein kinase activation. Here we use genetics, ABA-reporter imaging, stomatal conductance, patch clamp, and biochemical analyses to investigate these models. The strong ABA biosynthesis mutants nced3/nced5 and aba2-1 remain responsive to CO2 elevation. Rapid CO2-triggered stomatal closure in PYR/RCAR ABA receptor quadruple and hextuple mutants is not disrupted but delayed. Time-resolved ABA concentration monitoring in guard cells using a FRET-based ABA-reporter, ABAleon2.15, and ABA reporter gene assays suggest that CO2 elevation does not trigger [ABA] increases in guard cells, in contrast to control ABA exposures. Moreover, CO2 activates guard cell S-type anion channels in nced3/nced5 and ABA receptor hextuple mutants. Unexpectedly, in-gel protein kinase assays show that unlike ABA, elevated CO2 does not activate OST1/SnRK2 kinases in guard cells. The present study points to a model in which rapid CO2 signal transduction leading to stomatal closure occurs via an ABA-independent pathway downstream of OST1/SnRK2.6. Basal ABA signaling and OST1/SnRK2 activity are required to facilitate the stomatal response to elevated CO2. These findings provide insights into the interaction between CO2/ABA signal transduction in light of the continuing rise in atmospheric [CO2].

scholarly journals Role of Calcium in Signal Transduction of Commelina Guard Cells.

1991 ◽  
pp. 333-344 ◽  
Author(s):  
S. Gilroy ◽  
M. D. Fricker ◽  
N. D. Read ◽  
A. J. Trewavas
Keyword(s):  
Signal Transduction ◽  
Guard Cells

Ca2+ signalling in stomatal guard cells

2000 ◽  
Vol 28 (4) ◽  
pp. 476-481 ◽  
Author(s):  
M. R. McAinsh ◽  
J. E. Gray ◽  
A. M. Hetherington ◽  
C. P. Leckie ◽  
C. Ng
Keyword(s):  
Signal Transduction ◽  
Guard Cell ◽  
Signal Transduction Pathway ◽  
Guard Cells ◽  
Stomatal Opening ◽  
Cell Turgor ◽  
Stomatal Guard Cells ◽  
External Stimuli ◽  
Spatial And Temporal Characteristics

Ca2+ is a ubiquitous second messenger in the signal transduction pathway(s) by which stomatal guard cells respond to external stimuli. Increases in guard-cell cytosolic free Ca2+ concentration ([Ca2+]cyt) have been observed in response to stimuli that cause both stomatal opening and closure. In addition, several important components of Ca2+-based signalling pathways have been identified in guard cells, including the cADP-ribose and phospholipase C/Ins(1,4,5)P3-mediated Ca2+-mobilizing pathways. The central role of stimulus-induced increases in [Ca2+]cyt in guard-cell signal transduction has been clearly demonstrated in experiments examining the effects of modulating increases in [Ca2+]cyt on alterations in guard-cell turgor or the activity of ion channels that act as effectors in the guard-cell turgor response. In addition, the paradox that Ca2+ is involved in the transduction of signals that result in opposite end responses (stomatal opening and closure) might be accounted for by the generation of stimulus-specific Ca2+ signatures, such that increases in [Ca2+]cyt exhibit unique spatial and temporal characteristics.

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