The plant hormone cytokinin plays important roles in various aspects of plant growth and development. Cytokinin signaling is mediated by a multistep phosphorelay similar to bacterial two-component system. Type-B ARRs lie at the end of the cytokinin signaling, typically mediating the output response. However, it is still unclear how type-B ARRs are regulated in response to cytokinin. Typical type-B ARR contains an N-terminal receiver domain and a C-terminal effector domain. In this study, we performed a genome-wild comparative analysis by overexpressing full length and C-terminal effector domain of seven representative type-B ARRs. Our results indicated that overexpression of C-terminal effector domain causes short primary roots and short hypocotyls without the addition of cytokinin, suggesting that the inhibitory role of the receiver domain in the activity of the effector domain is a common mechanism in type-B ARRs. To investigate how the receiver domain inhibits the activity of the effector domain, we performed a deletion analysis. We found that deletion of the initial 45 residues of ARR18 (the 45 residues from N-terminus) causes pleiotropic growth defects by directly inducing cytokinin responsive genes. Together, our results suggest that the initial 45 residues are critical for the inhibitory role of the receiver domain to the effector domain in ARR18.
Copyright © 2012. Published by Elsevier Ltd.