摘要
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 compo- nents in the signaling pathway（s） leading to development of phototropic curvatures in hypocotyls. These include the pho- totropin photoreceptors （photl 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 coirradiated 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-mapl （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 auxl 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.
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 compo- nents in the signaling pathway（s） leading to development of phototropic curvatures in hypocotyls. These include the pho- totropin photoreceptors （photl 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 coirradiated 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-mapl （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 auxl 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.
基金
We thank Dr Malcolm Bennett for his generous contribution of various auxl missense alleles and for sharing unpublished results. Thanks also to members of the Liscum laboratory for review of the manuscript and critical suggestions to make presentation better. This work was supported by National Science Foundation Grant No. MCB-0077312, DBI-0114992, and IBN-0415970 to E.L.E.L.S.-E. was supported by a predoctoral fellowship from the University of Missouri Maize Biology Training Program, a unit of the US Department of Agriculture Collaborative Research in Plant Biology Program. R.B.C. was supported by predoctoral fellowships from the MU-MBRTI Program, MU-Monsanto Fellowship Program, and the MU Graduate School.
