Here, we report that the loss-of-function mutant of ANGUSTIFOLIA3 (AN3) delays asymmetric cell division... Furthermore, overexpression of AN3 accelerates asymmetric cell division...
First-pass extracted concept
ANGUSTIFOLIA3
Candidate: concept label1 source documents7 linked claims
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Aliases
AN3
Evidence Snippets
Supporting Sources
Linked Claims
Self-activation by AN3 contributes to control of AN3 expression.
Quoted textsource-backed
Self-activation by AN3 contributes to the control of AN3 expression.
Loss of function of AN3 delays asymmetric cell division and decreases stomatal index.
Quoted textsource-backed
Here, we report that the loss-of-function mutant of ANGUSTIFOLIA3 (AN3) delays asymmetric cell division, which leads to decreased stomatal index.
Overexpression of AN3 accelerates asymmetric cell division and results in clusters of stomata.
Quoted textsource-backed
Furthermore, overexpression of AN3 accelerates asymmetric cell division, which results in clusters of stomata.
AN3, COP1, and E3 ubiquitin ligase components form a regulatory complex that integrates light signaling into stomatal production and spacing.
Quoted textsource-backed
Together, these components for regulating stomatal development form an AN3-COP1-E3 ubiquitin ligase complex, allowing the integration of light signaling into the production and spacing of stomata.
AN3-regulated stomatal development is mediated by light signaling.
Quoted textsource-backed
In addition, the stomatal development through AN3 regulation is mediated by light signaling.
AN3 is associated with the COP1 promoter in regulation of light-controlling stomatal development.
Quoted textsource-backed
Target-gene analysis indicates that AN3 is associated with COP1 promoter for the regulation of light-controlling stomatal development.
AN3 is a light-signaling mutant and AN3 protein is light regulated.
Quoted textsource-backed
Finally, we find that an3 is a light-signaling mutant, and that AN3 protein is light regulated.