Minisymposium 10: Tropisms

Abs # 23003: Regulation of the root gravitropic response and basipetal auxin transport by the auxin efflux component Arabidopsis AGRAVITROPIC 1

Presenter:	Chen, Rujin , rchen@noble.org
Authors	Chen, Rujin  (A)   Shin, Heungsop  (A)   Shin, Hwa-Soo  (A)   Guo, Zibiao  (A)   Blancaflor, Elison B. (A)   Masson, Patrick H. (B)
Affiliations:	(A): Plant Biology Division, Samuel Roberts Noble Foundation, 2510 Sam Noble Pkw, Ardmore, OK 73401, USA (B): Laboratory of Genetics, University of Wisconsin-Madison

Polar auxin transport has been linked to many auxin-regulated processes including the gravitropic response in roots. We has previously shown that loss-of-function mutations in the Arabidopsis thaliana AGRAVITROPC 1 (AGR1) gene impair the root gravitropic response and the root basipetal auxin transport in the mutants. AGR1 gene is specifically expressed in the root meristem, and distal and central elongation zones (DEZ and CEZ), but not in the root cap columella cells. AGR1 protein is localized to the basal plasma membrane of epidermal, cortical and lateral cap cells. To elucidate regulatory mechanisms that underlie the AGR1 function, we compared the expression pattern of an auxin sensor/reporter DR5::GUS and the root basipetal auxin transport between wild type and agr1-5 mutant plants pre-treated with various chemicals. Our studies indicated that pre-treatment with exogenous-applied auxins readily induced the DR5::GUS gene expression in the CEZ cells of wild type plants. The auxin induction of the DR5::GUS gene expression in CEZ cells of the agr1-5 mutant was significantly delayed, suggesting a role of AGR1 in this response. Furthermore, the auxin-induced DR5::GUS expression in CEZ cells was blocked by cantharidin or okadaic acid, inhibitors of protein phosphatases 1 and 2A, and by 2,3,5-triiodobenzoic acid (TIBA), a polar auxin transport inhibitor. On the other hand, 1-naphthylphthalamic acid (NPA), a different polar auxin transport inhibitor, did not block the auxin-induced DR5::GUS expression in CEZ cells, suggesting a different mode of action by NPA. Cantharidin also reduced the root basipetal auxin transport and the gravitropic curvature response. In contrary, pre-treatment with brefeldin A, a vesicle trafficking inhibitor, did not block both the DR5::GUS expression in CEZ cells and the basipetal auxin transport, albeit it caused partial accumulation of the AGR1 protein in endosomal compartments in the epidermal and cortical cells of root tips. Taken together, our data suggest that protein phosphatases, targeted by cantharidin and/or okadaic acid are likely positive regulators of the activity of the auxin efflux component AGR1. On the other hand, BFA-sensitive vesicle trafficking may be required for the cycling of AGR1 between plasma membrane and BFA-compartments (Financial supports were from Noble Foundation to R.C. and E.B.B., and NASA to P.H.M.).