Source 1primary paper2002The Plant Cell
Toolkit/OST1
OST1
Also known as: Arabidopsis OST1 protein kinase, OST1, OST1 gene
Taxonomy: Mechanism Branch / Component. Workflows sit above the mechanism and technique branches rather than replacing them.
Summary
OST1 is an Arabidopsis thaliana protein kinase domain identified by positional cloning as an abscisic acid (ABA)-activated kinase expressed in stomatal guard cells and vascular tissue. Genetic and physiological evidence places OST1 as a regulator of stomatal movement, acting upstream of reactive oxygen species production and interacting genetically with HT1 during red light- and CO2-responsive stomatal responses.
Usefulness & Problems
Why this is useful
OST1 is useful as a signaling node for dissecting stomatal regulation by ABA, red light, and CO2 in Arabidopsis. The available evidence supports its use in functional assays that position kinase activity within guard-cell signaling pathways and test genetic interactions affecting stomatal aperture control.
Problem solved
OST1 helps address the problem of identifying where an ABA-responsive protein kinase functions within stomatal signaling cascades. Specifically, the evidence indicates that it links ABA-dependent signaling to downstream reactive oxygen species production and participates genetically in red light- and CO2-dependent stomatal movement responses with HT1.
Taxonomy & Function
Primary hierarchy
Mechanism Branch
Component: A low-level protein part used inside a larger architecture that realizes a mechanism.
Mechanisms
aba-dependent kinase activationgenetic interactionprotein phosphorylationsignal pathway positioning upstream of reactive oxygen species productionTechniques
Functional AssayTarget processes
signalingInput: Light
Implementation Constraints
The evidence indicates that OST1 was isolated by positional cloning and assessed using expression localization, in-gel kinase assays, and mutant functional analysis in Arabidopsis. Practical use therefore appears to depend on plant genetic backgrounds and stomatal aperture assays, but the supplied evidence does not specify construct design, cofactors beyond ABA-dependent activation context, or delivery methods.
The supplied evidence is limited to Arabidopsis and primarily to stomatal physiology and pathway inference rather than biochemical substrate identification. No quantitative performance metrics, structural information, domain boundaries, or heterologous implementation data are provided in the evidence set.
Validation
Cell-freeBacteriaMammalianMouseHumanTherapeuticIndep. Replication
Supporting Sources
Source 2primary paper2015New Phytologist
Ranked Claims
HT1 interacts genetically with OST1 during stomatal responses to red light and altered CO2.
HT1 was found to interact genetically with OST1 both during red light- and low [CO2 ]-induced stomatal opening. These results demonstrate that HT1 is essential for red light-induced stomatal opening and interacts genetically with OST1 during stomatal responses to red light and altered [CO2 ].
HT1 interacts genetically with OST1 during stomatal responses to red light and altered CO2.
HT1 was found to interact genetically with OST1 both during red light- and low [CO2 ]-induced stomatal opening. These results demonstrate that HT1 is essential for red light-induced stomatal opening and interacts genetically with OST1 during stomatal responses to red light and altered [CO2 ].
HT1 interacts genetically with OST1 during stomatal responses to red light and altered CO2.
HT1 was found to interact genetically with OST1 both during red light- and low [CO2 ]-induced stomatal opening. These results demonstrate that HT1 is essential for red light-induced stomatal opening and interacts genetically with OST1 during stomatal responses to red light and altered [CO2 ].
HT1 interacts genetically with OST1 during stomatal responses to red light and altered CO2.
HT1 was found to interact genetically with OST1 both during red light- and low [CO2 ]-induced stomatal opening. These results demonstrate that HT1 is essential for red light-induced stomatal opening and interacts genetically with OST1 during stomatal responses to red light and altered [CO2 ].
HT1 interacts genetically with OST1 during stomatal responses to red light and altered CO2.
HT1 was found to interact genetically with OST1 both during red light- and low [CO2 ]-induced stomatal opening. These results demonstrate that HT1 is essential for red light-induced stomatal opening and interacts genetically with OST1 during stomatal responses to red light and altered [CO2 ].
HT1 interacts genetically with OST1 during stomatal responses to red light and altered CO2.
HT1 was found to interact genetically with OST1 both during red light- and low [CO2 ]-induced stomatal opening. These results demonstrate that HT1 is essential for red light-induced stomatal opening and interacts genetically with OST1 during stomatal responses to red light and altered [CO2 ].
HT1 interacts genetically with OST1 during stomatal responses to red light and altered CO2.
HT1 was found to interact genetically with OST1 both during red light- and low [CO2 ]-induced stomatal opening. These results demonstrate that HT1 is essential for red light-induced stomatal opening and interacts genetically with OST1 during stomatal responses to red light and altered [CO2 ].
HT1 interacts genetically with OST1 during stomatal responses to red light and altered CO2.
HT1 was found to interact genetically with OST1 both during red light- and low [CO2 ]-induced stomatal opening. These results demonstrate that HT1 is essential for red light-induced stomatal opening and interacts genetically with OST1 during stomatal responses to red light and altered [CO2 ].
HT1 interacts genetically with OST1 during stomatal responses to red light and altered CO2.
HT1 was found to interact genetically with OST1 both during red light- and low [CO2 ]-induced stomatal opening. These results demonstrate that HT1 is essential for red light-induced stomatal opening and interacts genetically with OST1 during stomatal responses to red light and altered [CO2 ].
HT1 interacts genetically with OST1 during stomatal responses to red light and altered CO2.
HT1 was found to interact genetically with OST1 both during red light- and low [CO2 ]-induced stomatal opening. These results demonstrate that HT1 is essential for red light-induced stomatal opening and interacts genetically with OST1 during stomatal responses to red light and altered [CO2 ].
HT1 interacts genetically with OST1 during stomatal responses to red light and altered CO2.
HT1 was found to interact genetically with OST1 both during red light- and low [CO2 ]-induced stomatal opening. These results demonstrate that HT1 is essential for red light-induced stomatal opening and interacts genetically with OST1 during stomatal responses to red light and altered [CO2 ].
HT1 interacts genetically with OST1 during stomatal responses to red light and altered CO2.
HT1 was found to interact genetically with OST1 both during red light- and low [CO2 ]-induced stomatal opening. These results demonstrate that HT1 is essential for red light-induced stomatal opening and interacts genetically with OST1 during stomatal responses to red light and altered [CO2 ].
Applied hydrogen peroxide or calcium elicits the same degree of stomatal closure in ost1 mutants as in wild type, suggesting OST1 acts between ABA perception and ROS production.
applied H(2)O(2) or calcium elicited the same degree of stomatal closure in ost1 as in the wild type. These results suggest that OST1 acts in the interval between ABA perception and ROS production.
Applied hydrogen peroxide or calcium elicits the same degree of stomatal closure in ost1 mutants as in wild type, suggesting OST1 acts between ABA perception and ROS production.
applied H(2)O(2) or calcium elicited the same degree of stomatal closure in ost1 as in the wild type. These results suggest that OST1 acts in the interval between ABA perception and ROS production.
Applied hydrogen peroxide or calcium elicits the same degree of stomatal closure in ost1 mutants as in wild type, suggesting OST1 acts between ABA perception and ROS production.
applied H(2)O(2) or calcium elicited the same degree of stomatal closure in ost1 as in the wild type. These results suggest that OST1 acts in the interval between ABA perception and ROS production.
Applied hydrogen peroxide or calcium elicits the same degree of stomatal closure in ost1 mutants as in wild type, suggesting OST1 acts between ABA perception and ROS production.
applied H(2)O(2) or calcium elicited the same degree of stomatal closure in ost1 as in the wild type. These results suggest that OST1 acts in the interval between ABA perception and ROS production.
Applied hydrogen peroxide or calcium elicits the same degree of stomatal closure in ost1 mutants as in wild type, suggesting OST1 acts between ABA perception and ROS production.
applied H(2)O(2) or calcium elicited the same degree of stomatal closure in ost1 as in the wild type. These results suggest that OST1 acts in the interval between ABA perception and ROS production.
Applied hydrogen peroxide or calcium elicits the same degree of stomatal closure in ost1 mutants as in wild type, suggesting OST1 acts between ABA perception and ROS production.
applied H(2)O(2) or calcium elicited the same degree of stomatal closure in ost1 as in the wild type. These results suggest that OST1 acts in the interval between ABA perception and ROS production.
Applied hydrogen peroxide or calcium elicits the same degree of stomatal closure in ost1 mutants as in wild type, suggesting OST1 acts between ABA perception and ROS production.
applied H(2)O(2) or calcium elicited the same degree of stomatal closure in ost1 as in the wild type. These results suggest that OST1 acts in the interval between ABA perception and ROS production.
OST1 is expressed in stomatal guard cells and vascular tissue.
The OST1 gene was isolated by positional cloning and was found to be expressed in stomatal guard cells and vascular tissue.
OST1 is expressed in stomatal guard cells and vascular tissue.
The OST1 gene was isolated by positional cloning and was found to be expressed in stomatal guard cells and vascular tissue.
OST1 is expressed in stomatal guard cells and vascular tissue.
The OST1 gene was isolated by positional cloning and was found to be expressed in stomatal guard cells and vascular tissue.
OST1 is expressed in stomatal guard cells and vascular tissue.
The OST1 gene was isolated by positional cloning and was found to be expressed in stomatal guard cells and vascular tissue.
OST1 is expressed in stomatal guard cells and vascular tissue.
The OST1 gene was isolated by positional cloning and was found to be expressed in stomatal guard cells and vascular tissue.
OST1 is expressed in stomatal guard cells and vascular tissue.
The OST1 gene was isolated by positional cloning and was found to be expressed in stomatal guard cells and vascular tissue.
OST1 is expressed in stomatal guard cells and vascular tissue.
The OST1 gene was isolated by positional cloning and was found to be expressed in stomatal guard cells and vascular tissue.
OST1 is an ABA-activated protein kinase related to Vicia faba AAPK.
In-gel assays indicated that OST1 is an ABA-activated protein kinase related to the Vicia faba ABA-activated protein kinase (AAPK).
OST1 is an ABA-activated protein kinase related to Vicia faba AAPK.
In-gel assays indicated that OST1 is an ABA-activated protein kinase related to the Vicia faba ABA-activated protein kinase (AAPK).
OST1 is an ABA-activated protein kinase related to Vicia faba AAPK.
In-gel assays indicated that OST1 is an ABA-activated protein kinase related to the Vicia faba ABA-activated protein kinase (AAPK).
OST1 is an ABA-activated protein kinase related to Vicia faba AAPK.
In-gel assays indicated that OST1 is an ABA-activated protein kinase related to the Vicia faba ABA-activated protein kinase (AAPK).
OST1 is an ABA-activated protein kinase related to Vicia faba AAPK.
In-gel assays indicated that OST1 is an ABA-activated protein kinase related to the Vicia faba ABA-activated protein kinase (AAPK).
OST1 is an ABA-activated protein kinase related to Vicia faba AAPK.
In-gel assays indicated that OST1 is an ABA-activated protein kinase related to the Vicia faba ABA-activated protein kinase (AAPK).
OST1 is an ABA-activated protein kinase related to Vicia faba AAPK.
In-gel assays indicated that OST1 is an ABA-activated protein kinase related to the Vicia faba ABA-activated protein kinase (AAPK).
ost1 mutations do not affect stomatal regulation by light or CO2, supporting a specific role for OST1 in ABA signaling.
the ost1 mutations did not affect stomatal regulation by light or CO(2), suggesting that OST1 is involved specifically in ABA signaling
ost1 mutations do not affect stomatal regulation by light or CO2, supporting a specific role for OST1 in ABA signaling.
the ost1 mutations did not affect stomatal regulation by light or CO(2), suggesting that OST1 is involved specifically in ABA signaling
ost1 mutations do not affect stomatal regulation by light or CO2, supporting a specific role for OST1 in ABA signaling.
the ost1 mutations did not affect stomatal regulation by light or CO(2), suggesting that OST1 is involved specifically in ABA signaling
ost1 mutations do not affect stomatal regulation by light or CO2, supporting a specific role for OST1 in ABA signaling.
the ost1 mutations did not affect stomatal regulation by light or CO(2), suggesting that OST1 is involved specifically in ABA signaling
ost1 mutations do not affect stomatal regulation by light or CO2, supporting a specific role for OST1 in ABA signaling.
the ost1 mutations did not affect stomatal regulation by light or CO(2), suggesting that OST1 is involved specifically in ABA signaling
ost1 mutations do not affect stomatal regulation by light or CO2, supporting a specific role for OST1 in ABA signaling.
the ost1 mutations did not affect stomatal regulation by light or CO(2), suggesting that OST1 is involved specifically in ABA signaling
ost1 mutations do not affect stomatal regulation by light or CO2, supporting a specific role for OST1 in ABA signaling.
the ost1 mutations did not affect stomatal regulation by light or CO(2), suggesting that OST1 is involved specifically in ABA signaling
Approval Evidence
2 sources5 linked approval claimsfirst-pass slugs open-stomata-1, ost1
OPEN STOMATA 1 (OST1)
Source:
The OST1 gene was isolated by positional cloning and was found to be expressed in stomatal guard cells and vascular tissue. In-gel assays indicated that OST1 is an ABA-activated protein kinase
Source:
genetic interactionsupports
HT1 interacts genetically with OST1 during stomatal responses to red light and altered CO2.
HT1 was found to interact genetically with OST1 both during red light- and low [CO2 ]-induced stomatal opening. These results demonstrate that HT1 is essential for red light-induced stomatal opening and interacts genetically with OST1 during stomatal responses to red light and altered [CO2 ].
Source:
epistasis inferencesupports
Applied hydrogen peroxide or calcium elicits the same degree of stomatal closure in ost1 mutants as in wild type, suggesting OST1 acts between ABA perception and ROS production.
applied H(2)O(2) or calcium elicited the same degree of stomatal closure in ost1 as in the wild type. These results suggest that OST1 acts in the interval between ABA perception and ROS production.
Source:
expression localizationsupports
OST1 is expressed in stomatal guard cells and vascular tissue.
The OST1 gene was isolated by positional cloning and was found to be expressed in stomatal guard cells and vascular tissue.
Source:
molecular functionsupports
OST1 is an ABA-activated protein kinase related to Vicia faba AAPK.
In-gel assays indicated that OST1 is an ABA-activated protein kinase related to the Vicia faba ABA-activated protein kinase (AAPK).
Source:
pathway specificitysupports
ost1 mutations do not affect stomatal regulation by light or CO2, supporting a specific role for OST1 in ABA signaling.
the ost1 mutations did not affect stomatal regulation by light or CO(2), suggesting that OST1 is involved specifically in ABA signaling
Source:
Comparisons
Source-backed strengths
OST1 has direct evidence for guard-cell and vascular expression, ABA-activated kinase behavior in in-gel assays, and pathway placement from mutant physiological responses. Its function is supported by two source studies spanning ABA signaling and red light/CO2 stomatal responses, including genetic interaction evidence with HT1.
Ranked Citations
- 1.
- 2.