Auxins are plant hormones that mediate many aspects of plant growth and development. In higher plants, auxins are polarly transported from sites of synthesis in the shoot apex to their sites of action in the basal regions of shoots and in roots. Polar auxin transport is an important aspect of auxin functions and is mediated by cellular inf lux and eff lux carriers. Little is known about the molecular identity of its regulatory component, the eff lux carrier [Estelle, M. (1996) Current Biol. 6, 1589-1591]. Here we show that mutations in the Arabidopsis thaliana AGRAVITROPIC 1 (AGR1) gene involved in root gravitropism confer increased root-growth sensitivity to auxin and decreased sensitivity to ethylene and an auxin transport inhibitor, and cause retention of exogenously added auxin in root tip cells. We used positional cloning to show that AGR1 encodes a putative transmembrane protein whose amino acid sequence shares homologies with bacterial transporters. When expressed in Saccharomyces cerevisiae, AGR1 promotes an increased eff lux of radiolabeled IAA from the cells and confers increased resistance to f luoro-IAA, a toxic IAA-derived compound. AGR1 transcripts were localized to the root distal elongation zone, a region undergoing a curvature response upon gravistimulation. We have identified several AGR1-related genes in Arabidopsis, suggesting a global role of this gene family in the control of auxin-regulated growth and developmental processes.Plant roots typically grow downward, at a defined angle from the gravity vector. They respond to deviations from the defined growth angle (gravistimulation) by developing a curvature at the distal and central elongation zones, which eventually allows their tip to resume a normal growth pattern. The gravitropic response involves perception of the gravistimulus by the root cap columella cells, transduction of that physical information into physiological signals, transmission of the signals to the distal and central elongation zones, and curvature response (1). Physiological evidence suggests that auxin and, possibly, apoplastic Ca 2ϩ constitute the physiological signals that are transmitted to the root distal and central elongation zones and are responsible for the curvature response (1).Basipetal transmission of auxin is mediated by polar auxin transport machinery, which involve influx and efflux carriers. The polarity of auxin transport probably is established by a basal localization of the efflux carrier in transporting cells (2). In this report, we demonstrate that the Arabidopsis thaliana AGR1 gene encodes a component of the auxin efflux carrier that mediates the root gravitropic response. MATERIALS AND METHODSPlant Stocks. The following alleles were analyzed and found to belong to the same complementation group: agr1-1, agr1-2, agr1-3 (Landsberg erecta; previously named as agr-1, agr-2, and agr-3, respectively) (3), agr1-4 (Wassilewskija; WS), agr1 , wav6 (Landsberg; agr1-52) (4), and eir1-1 (Columbia) (5). Manipulation of plant stocks was described previou...

No abstract

The arl2 mutants of Arabidopsis display altered root and hypocotyl gravitropism, whereas their inflorescence stems are fully gravitropic. Interestingly, mutant roots respond like the wild type to phytohormones and an inhibitor of polar auxin transport. Also, their cap columella cells accumulate starch similarly to wild-type cells, and mutant hypocotyls display strong phototropic responses to lateral light stimulation. The ARL2 gene encodes a DnaJ-like protein similar to ARG1, another protein previously implicated in gravity signal transduction in Arabidopsis seedlings. ARL2 is expressed at low levels in all organs of seedlings and plants. arl2-1 arg1-2 double mutant roots display kinetics of gravitropism similar to those of single mutants. However, double mutants carrying both arl2-1 and pgm-1 (a mutation in the starch-biosynthetic gene PHOSPHOGLUCOMUTASE) at the homozygous state display a more pronounced root gravitropic defect than the single mutants. On the other hand, seedlings with a null mutation in ARL1, a paralog of ARG1 and ARL2, behave similarly to the wild type in gravitropism and other related assays. Taken together, the results suggest that ARG1 and ARL2 function in the same gravity signal transduction pathway in the hypocotyl and root of Arabidopsis seedlings, distinct from the pathway involving PGM.Gravity is one of the environmental cues that guides plant organs' growth. Most plant organs are characterized by a specific gravity set point angle, which defines their preferential growth vector relative to gravity (Firn and Digby, 1997). In young Arabidopsis seedlings, shoots grow upward, displaying negative gravitropism, whereas roots grow downward, toward the center of gravity (positive gravitropism; Bullen et al., 1990;Boonsirichai et al., 2002).Gravity perception by dicot organs involves primarily the sedimentation of amyloplasts within specialized cells (statocytes) located in the columella region of the root cap and in the starch sheath, which constitutes the endodermis of hypocotyls and inflorescence stems (Kiss et al., 1996;Kuznetsov and Hasenstein, 1996;Blancaflor et al., 1998; Weise et al., 2000). In shoots, sedimentable amyloplasts and the curvature response to gravistimulation occur along the elongation zone (for review, see Masson et al., 2002). After amyloplast sedimentation, signals are likely transduced within the endodermal cells, and physiological signals are transported laterally to affect elongation of cortical and epidermal cells. In roots, sites of gravity perception and curvature response may be physically separated (Poff and Martin, 1989). Hence, physiological signals resulting from activation of the gravity signal transduction pathway should be transported from the root cap columella to the elongation zones where the gravitropic curvature is initiated (for review, see Boonsirichai et al., 2002).Auxin is a physiological signal that has been shown to mediate the gravitropic response (for review, see Masson et al., 2002). In gravistimulated roots, auxin is redistributed asymmet...

No abstract

No abstract