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Published on April 10, 2009; 10.1104/pp.108.131607

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Received October 23, 2008
Accepted April 7, 2009

PINOID kinase regulates root gravitropism through modulation of PIN2-dependent basipetal auxin transport in Arabidopsis thaliana

Poornima Sukumar , Karin S. Edwards , Abidur Rahman , Alison DeLong , and Gloria K. Muday *

Department of Biology, Wake Forest University, Winston-Salem, NC 27109; Cryobiofrontier Research Center, Iwate University, Ueda, Japan; Department of Molecular Biology, Cell Biology, and Biochemistry, Brown University, Providence, RI 02912

* Corresponding author; email: muday{at}wfu.edu.

Reversible protein phosphorylation is a key regulatory mechanism governing polar auxin transport. We characterized the auxin transport and gravitropic phenotypes of the pinoid-9 mutant and tested the hypothesis that PINOID (PID)-mediated phosphorylation and RCN1-regulated dephosphorylation might antagonistically regulate root auxin transport and gravity response. Basipetal IAA transport and gravitropism are reduced in pid-9 seedlings, while acropetal transport and lateral root development are unchanged. Treatment of wild-type seedlings with the protein kinase inhibitor staurosporine phenocopies the reduced auxin transport and gravity response of pid-9, while pid-9 is resistant to inhibition by staurosporine. Staurosporine and the phosphatase inhibitor, cantharidin, delay the asymmetry of DR5::revGFP expression at the root tip after gravistimulation. Gravity response defects of rcn1 and pid-9 are partially rescued by treatment with staurosporine or cantharidin, respectively. The pid-9 rcn1 double mutant has a more rapid gravitropic response than rcn1. These data are consistent with a reciprocal regulation of gravitropism by RCN1 and PID. Furthermore, the effect of staurosporine is lost in pin2. Our data suggest that reduced PID kinase function inhibits gravitropism and basipetal IAA transport. However, in contrast to PID overexpression studies, we observed wild-type asymmetric membrane distribution of the PIN2 protein in both pid-9 and wild-type root tips, although PIN2 accumulates in endomembrane structures in pid-9 roots. Similarly, staurosporine-treated plants expressing a PIN2::GFP fusion exhibit endomembrane accumulation of PIN2::GFP, but no changes in membrane asymmetries were detected. Our data suggest that PID plays a limited role in root development; loss of PID activity alters auxin transport and gravitropism without causing an obvious change in cellular polarity.






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