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Published on January 28, 2005; 10.1104/pp.104.049577


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Received July 9, 2004
Returned for revision August 18, 2004
Accepted November 23, 2004

An Auxin Transport Independent Pathway Is Involved in Phosphate Stress-Induced Root Architectural Alterations in Arabidopsis. Identification of BIG as a Mediator of Auxin in Pericycle Cell Activation

José López-Bucio , Esmeralda Hernández-Abreu , Lenin Sánchez-Calderón , Anahí Pérez-Torres , Rebekah A. Rampey , Bonnie Bartel , and Luis Herrera-Estrella *

Departamento de Ingeniería Genética, Unidad Irapuato del Centro de Investigación y Estudios Avanzados del Instituto Politécnico Nacional, 36500 Irapuato, Guanajuato, Mexico
Department of Biochemistry and Cell Biology, Rice University, Houston, Texas 77005-1892

* Corresponding author; email: lherrera{at}ira.cinvestav.mx.

Arabidopsis (Arabidopsis thaliana) plants display a number of root developmental responses to low phosphate availability, including primary root growth inhibition, greater formation of lateral roots, and increased root hair elongation. To gain insight into the regulatory mechanisms by which phosphorus (P) availability alters postembryonic root development, we performed a mutant screen to identify genetic determinants involved in the response to P deprivation. Three low phosphate-resistant root lines (lpr1-1 to lpr1-3) were isolated because of their reduced lateral root formation in low P conditions. Genetic and molecular analyses revealed that all lpr1 mutants were allelic to BIG, which is required for normal auxin transport in Arabidopsis. Detailed characterization of lateral root primordia (LRP) development in wild-type and lpr1 mutants revealed that BIG is required for pericycle cell activation to form LRP in both high (1 mM) and low (1 µM) P conditions, but not for the low P-induced alterations in primary root growth, lateral root emergence, and root hair elongation. Exogenously supplied auxin restored normal lateral root formation in lpr1 mutants in the two P treatments. Treatment of wild-type Arabidopsis seedlings with brefeldin A, a fungal metabolite that blocks auxin transport, phenocopies the root developmental alterations observed in lpr1 mutants in both high and low P conditions, suggesting that BIG participates in vesicular targeting of auxin transporters. Taken together, our results show that auxin transport and BIG function have fundamental roles in pericycle cell activation to form LRP and promote root hair elongation. The mechanism that activates root system architectural alterations in response to P deprivation, however, seems to be independent of auxin transport and BIG.




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