Molecular Plant Advance Access originally published online on October 24, 2007
Molecular Plant 2008 1(1):129-144; doi:10.1093/mp/ssm013
| ||||||||||||||||||||||||||||||||||||||||||||||||||||
© The Author 2007. Published by Oxford University Press on behalf of CSPP and IPPE, SIBS, CAS.
Disruptions in AUX1-Dependent Auxin Influx Alter Hypocotyl Phototropism in Arabidopsis
a Division of Biological Sciences, University of Missouri, Columbia, Missouri 65211, USA
b Christopher S. Bond Life Sciences Center, University of Missouri, Columbia, Missouri 65211, USA
c Department of Forest Genetics and Plant Physiology, Umeå Plant Science Center, SE-90183 Umeå, Sweden
1 To whom correspondence should be addressed at Room 371 E, address (b). E-mail liscume{at}missouri.edu, fax 573–882–1023.
Phototropism represents a differential growth response by which plant organs can respond adaptively to changes in the direction of incident light to optimize leaf/stem positioning for photosynthetic light capture and root growth orientation for water/nutrient acquisition. Studies over the past few years have identified a number of components in the signaling pathway(s) leading to development of phototropic curvatures in hypocotyls. These include the phototropin photoreceptors (phot1 and phot2) that perceive directional blue-light (BL) cues and then stimulate signaling, leading to relocalization of the plant hormone auxin, as well as the auxin response factor NPH4/ARF7 that responds to changes in local auxin concentrations to directly mediate expression of genes likely encoding proteins necessary for development of phototropic curvatures. While null mutations in NPH4/ARF7 condition an aphototropic response to unidirectional BL, seedlings carrying the same mutations recover BL-dependent phototropic responsiveness if co-irradiated with red light (RL) or pre-treated with either ethylene. In the present study, we identify second-site enhancer mutations in the nph4 background that abrogate these recovery responses. One of these mutations—map1 (modifier of arf7 phenotypes 1)—was found to represent a missense allele of AUX1—a gene encoding a high-affinity auxin influx carrier previously associated with a number of root responses. Pharmocological studies and analyses of additional aux1 mutants confirmed that AUX1 functions as a modulator of hypocotyl phototropism. Moreover, we have found that the strength of dependence of hypocotyl phototropism on AUX1-mediated auxin influx is directly related to the auxin responsiveness of the seedling in question.
2 Current address: Biology Department, Bucknell University, Lewisburg, Pennsylvania 17837, USA.