Plant Cell Advance Online Publication Published on June 8, 2007; 10.1105/tpc.107.051599
OPEN ACCESS ARTICLE
Received March 13, 2007
Returned for revision May 7, 2007
Accepted May 15, 2007
Separating the Roles of Acropetal and Basipetal Auxin Transport on Gravitropism with Mutations in Two Arabidopsis Multidrug Resistance-Like ABC Transporter Genes
Daniel R. Lewis 1, Nathan D. Miller 2, Bessie L. Splitt 1, Guosheng Wu 1, and Edgar P. Spalding 3*
1 Department of Botany, University of Wisconsin, Madison, Wisconsin 53706
2 Department of Biomedical Engineering, University of Wisconsin, Madison, Wisconsin 53706
3 Department of Botany, University of Wisconsin, Madison, Wisconsin 53706; Department of Biomedical Engineering, University of Wisconsin, Madison, Wisconsin 53706
* To whom correspondence should be addressed. E-mail: spalding{at}wisc.edu.
Two Arabidopsis thaliana ABC transporter genes linked to auxin transport by various previous results were studied in a reverse-genetic fashion. Mutations in Multidrug Resistance-Like1 (MDR1) reduced acropetal auxin transport in roots by 80% without affecting basipetal transport. Conversely, mutations in MDR4 blocked 50% of basipetal transport without affecting acropetal transport. Developmental and auxin distribution phenotypes associated with these altered auxin flows were studied with a high-resolution morphometric system and confocal microscopy, respectively. Vertically grown mdr1 roots produced positive and negative curvatures threefold greater than the wild type, possibly due to abnormal auxin distribution observed in the elongation zone. However, upon 90° reorientation, mdr1 gravitropism was inseparable from the wild type. Thus, acropetal auxin transport maintains straight growth but contributes surprisingly little to gravitropism. Conversely, vertically maintained mdr4 roots grew as straight as the wild type, but their gravitropism was enhanced. Upon reorientation, curvature in this mutant developed faster, was distributed more basally, and produced a greater total angle than the wild type. An amplified auxin asymmetry may explain the mdr4 hypertropism. Double mutant analysis indicated that the two auxin transport streams are more independent than interdependent. The hypothesis that flavanols regulate MDR-dependent auxin transport was supported by the epistatic relationship of mdr4 to the tt4 phenylpropanoid pathway mutation.
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