Cytokinin modulates endocytic trafficking of PIN1 auxin efflux carrier to control plant organogenesis Journal Article


Author(s): Marhavý, Peter; Bielach, Agnieszka; Abas, Lindy; Abuzeineh, Anas; Duclercq, Jérôme; Tanaka, Hirokazu; Pařezová, Markéta; Petrášek, Jan; Friml, Jiří; Kleine-Vehn, Jürgen; Benková, Eva
Article Title: Cytokinin modulates endocytic trafficking of PIN1 auxin efflux carrier to control plant organogenesis
Affiliation
Abstract: Cytokinin is an important regulator of plant growth and development. In Arabidopsis thaliana, the two-component phosphorelay mediated through a family of histidine kinases and response regulators is recognized as the principal cytokinin signal transduction mechanism activating the complex transcriptional response to control various developmental processes. Here, we identified an alternative mode of cytokinin action that uses endocytic trafficking as a means to direct plant organogenesis. This activity occurs downstream of known cytokinin receptors but through a branch of the cytokinin signaling pathway that does not involve transcriptional regulation. We show that cytokinin regulates endocytic recycling of the auxin efflux carrier PINFORMED1 (PIN1) by redirecting it for lytic degradation in vacuoles. Stimulation of the lytic PIN1 degradation is not a default effect for general downregulation of proteins from plasma membranes, but a specific mechanism to rapidly modulate the auxin distribution in cytokinin-mediated developmental processes.
Keywords: Reverse Transcriptase Polymerase Chain Reaction; Blotting, Western; Protein Transport; plant roots; Endocytosis; Gene Expression Regulation, Plant; RNA, Messenger; Organogenesis; Arabidopsis; Arabidopsis Proteins; Indoleacetic Acids; Cell Membrane; Membrane Transport Proteins; Plant Growth Regulators; RNA, Plant; Vacuoles; Cytokinins; Seeds
Journal Title: Developmental Cell
Volume: 21
Issue 4
ISSN: 1534-5807
Publisher: Cell Press  
Date Published: 2011-10-18
Start Page: 796
End Page: 804
DOI: 10.1016/j.devcel.2011.08.014
Open access: no