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Systems dynamic modeling of a guard cell Cl- channel mutant uncovers an emergent homeostatic network regulating stomatal transpiration.

Plant Physiol.2012 Dec;160(4):1956-67. Epub 2012 Oct 22
Yizhou Wang 1 , Maria Papanatsiou , Cornelia Eisenach , Rucha Karnik , Mary Williams , Adrian Hills , Virgilio L Lew , Michael R Blatt
Yizhou Wang 1 , Maria Papanatsiou , Cornelia Eisenach , Rucha Karnik , Mary Williams , Adrian Hills , Virgilio L Lew , Michael R Blatt
+ et al

[No authors listed]

Author information
  • 1 Laboratory of Plant Physiology and Biophysics, Institute of Molecular, Cell, and Systems Biology, University of Glasgow, Glasgow G12 8QQ, United Kingdom.

摘要


Stomata account for much of the 70% of global water usage associated with agriculture and have a profound impact on the water and carbon cycles of the world. Stomata have long been modeled mathematically, but until now, no systems analysis of a plant cell has yielded detail sufficient to guide phenotypic and mutational analysis. Here, we demonstrate the predictive power of a systems dynamic model in Arabidopsis (Arabidopsis thaliana) to explain the paradoxical suppression of channels that facilitate K(+) uptake, slowing stomatal opening, by mutation of the SLAC1 anion channel, which mediates solute loss for closure. The model showed how anion accumulation in the mutant suppressed the H(+) load on the cytosol and promoted Ca(2+) influx to elevate cytosolic pH (pH(i)) and free cytosolic Ca(2+) concentration ([Ca(2+)](i)), in turn regulating the K(+) channels. We have confirmed these predictions, measuring pH(i) and [Ca(2+)](i) in vivo, and report that experimental manipulation of pH(i) and [Ca(2+)](i) is sufficient to recover K(+) channel activities and accelerate stomatal opening in the slac1 mutant. Thus, we uncover a previously unrecognized signaling network that ameliorates the effects of the slac1 mutant on transpiration by regulating the K(+) channels. Additionally, these findings underscore the importance of H(+)-coupled anion transport for pH(i) homeostasis.