Interestingly, a mutant has been identified in a gene encoding the regulatory A subunit of a trimeric protein phosphatase 2A (PP2A), that displays root curling in response to NPA (rcnl) (Garbers et al. 1996). The rcnl mutant shows increased root basipetal auxin transport, reduced gravitropic response and a delay in the establishment of differential auxin-induced gene expression across a gravity-stimulated root tip, aspects that were restored to normal upon NPA treatment (Rashotte et al. 2001). Michniewicz and co-workers showed that PP2A activity, of which RCN1 is one of the three regulatory A subunits (PP2AA) in Arabidopsis, antagonizes the action of PID on PINs. PP2AA loss-of-function resulted in the same basal-to-apical switches in PIN polarity, leading to similar embryo and root defects as PID overexpression, whereas the pid mutation partially suppressed these pp2aa loss-of-function phenotypes. Moreover, both PID and PP2AA partially co-localize with PIN proteins on the plasma membrane, and in vivo and semi in vivo phospho-rylation assays showed that they act antagonistically on the phosphorylation status of PIN proteins (Michniewicz et al. 2007). This beautifully exemplifies a dual molecular switch in which PID-mediated phosphorylation of PINs induces apical localization of these efflux carriers, resulting in upward PAT, while PP2A-mediated dephosphorylation of PINs reverses this situation, consequently resulting in downward PAT (Fig. 2).
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