Light signals are perceived by multiple photoreceptors that converge to suppress theRING E3 ubiquitin ligase CONSTITUTIVE PHOTOMORPHOGENIC1 (COP1) for theregulation of stomatal development. Thus, COP1 is a point of integration betweenlight signaling and stomatal patterning. However, how light signaling is collected intoCOP1 for the production and spacing of stomata is still unknown. Here, we reportthat the loss‐of‐function mutant of ANGUSTIFOLIA3 (AN3) delays asymmetric celldivision, which leads to decreased stomatal index. Furthermore, overexpression ofAN3 accelerates asymmetric cell division, which results in clusters of stomata. In addi-tion, the stomatal development through AN3 regulation is mediated by light signaling.Finally, we find that an3 is a light‐signaling mutant, and that AN3 protein is light reg-ulated. Self‐activation by AN3 contributes to the control of AN3 expression. Thus,AN3 is a point of collection between light signaling and stomatal patterning. Target‐gene analysis indicates that AN3 is associated with COP1 promoter for the regulationof light‐controlling stomatal development. Together, these components for regulatingstomatal development form an AN3–COP1–E3 ubiquitin ligase complex, allowing theintegration of light signaling into the production and spacing of stomata.