dorsal/arxiv
View SchemaPredicting essential components of signal transduction networks: a dynamic model of guard cell abscisic acid signaling
| Authors | Song Li, Sarah M. Assmann, Reka Albert |
|---|---|
| Categories | |
| ArXiv ID | q-bio/0610012 |
| URL | https://arxiv.org/abs/q-bio/0610012 |
| DOI | 10.1371/journal.pbio.0040312 |
| Journal | PLoS Biology 4 (10), e312 (2006) |
Abstract
Plants both lose water and take in carbon dioxide through microscopic stomatal pores, each of which is regulated by a surrounding pair of guard cells. During drought, the plant hormone abscisic acid (ABA) inhibits stomatal opening and promotes stomatal closure, thereby promoting water conservation. Here we synthesize experimental results into a consistent guard cell signal transduction network for ABA-induced stomatal closure, and develop a dynamic model of this process. Our model captures the regulation of more than forty identified network components, and accords well with previous experimental results at both the pathway and whole cell physiological level. Our analysis reveals the novel predictions that the disruption of membrane depolarizability, anion efflux, actin cytoskeleton reorganization, cytosolic pH increase, the phosphatidic acid pathway or of K+ efflux through slowly activating K+ channels at the plasma membrane lead to the strongest reduction in ABA responsiveness. Initial experimental analysis assessing ABA-induced stomatal closure in the presence of cytosolic pH clamp imposed by the weak acid butyrate is consistent with model prediction. Our method can be readily applied to other biological signaling networks to identify key regulatory components in systems where quantitative information is limited.
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"abstract": "Plants both lose water and take in carbon dioxide through microscopic\nstomatal pores, each of which is regulated by a surrounding pair of guard\ncells. During drought, the plant hormone abscisic acid (ABA) inhibits stomatal\nopening and promotes stomatal closure, thereby promoting water conservation.\nHere we synthesize experimental results into a consistent guard cell signal\ntransduction network for ABA-induced stomatal closure, and develop a dynamic\nmodel of this process. Our model captures the regulation of more than forty\nidentified network components, and accords well with previous experimental\nresults at both the pathway and whole cell physiological level. Our analysis\nreveals the novel predictions that the disruption of membrane depolarizability,\nanion efflux, actin cytoskeleton reorganization, cytosolic pH increase, the\nphosphatidic acid pathway or of K+ efflux through slowly activating K+ channels\nat the plasma membrane lead to the strongest reduction in ABA responsiveness.\nInitial experimental analysis assessing ABA-induced stomatal closure in the\npresence of cytosolic pH clamp imposed by the weak acid butyrate is consistent\nwith model prediction. Our method can be readily applied to other biological\nsignaling networks to identify key regulatory components in systems where\nquantitative information is limited.",
"arxiv_id": "q-bio/0610012",
"authors": [
"Song Li",
"Sarah M. Assmann",
"Reka Albert"
],
"categories": [
"q-bio.MN",
"q-bio.SC"
],
"doi": "10.1371/journal.pbio.0040312",
"journal_ref": "PLoS Biology 4 (10), e312 (2006)",
"title": "Predicting essential components of signal transduction networks: a dynamic model of guard cell abscisic acid signaling",
"url": "https://arxiv.org/abs/q-bio/0610012"
},
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