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• W2024692287 abstract "Article15 April 1999free access AUX1 regulates root gravitropism in Arabidopsis by facilitating auxin uptake within root apical tissues Alan Marchant Alan Marchant Division of Plant Sciences, School of Biological Sciences, University of Nottingham, NG7 2RD UK Search for more papers by this author Joanna Kargul Joanna Kargul Division of Plant Sciences, School of Biological Sciences, University of Nottingham, NG7 2RD UK Search for more papers by this author Sean T. May Sean T. May Division of Plant Sciences, School of Biological Sciences, University of Nottingham, NG7 2RD UK Search for more papers by this author Philippe Muller Philippe Muller Institut des Sciences Végétales, CNRS, 91198 Gif-sur-Yvette, Cedex, France Search for more papers by this author Alain Delbarre Alain Delbarre Institut des Sciences Végétales, CNRS, 91198 Gif-sur-Yvette, Cedex, France Search for more papers by this author Catherine Perrot-Rechenmann Catherine Perrot-Rechenmann Institut des Sciences Végétales, CNRS, 91198 Gif-sur-Yvette, Cedex, France Search for more papers by this author Malcolm J. Bennett Corresponding Author Malcolm J. Bennett Division of Plant Sciences, School of Biological Sciences, University of Nottingham, NG7 2RD UK Search for more papers by this author Alan Marchant Alan Marchant Division of Plant Sciences, School of Biological Sciences, University of Nottingham, NG7 2RD UK Search for more papers by this author Joanna Kargul Joanna Kargul Division of Plant Sciences, School of Biological Sciences, University of Nottingham, NG7 2RD UK Search for more papers by this author Sean T. May Sean T. May Division of Plant Sciences, School of Biological Sciences, University of Nottingham, NG7 2RD UK Search for more papers by this author Philippe Muller Philippe Muller Institut des Sciences Végétales, CNRS, 91198 Gif-sur-Yvette, Cedex, France Search for more papers by this author Alain Delbarre Alain Delbarre Institut des Sciences Végétales, CNRS, 91198 Gif-sur-Yvette, Cedex, France Search for more papers by this author Catherine Perrot-Rechenmann Catherine Perrot-Rechenmann Institut des Sciences Végétales, CNRS, 91198 Gif-sur-Yvette, Cedex, France Search for more papers by this author Malcolm J. Bennett Corresponding Author Malcolm J. Bennett Division of Plant Sciences, School of Biological Sciences, University of Nottingham, NG7 2RD UK Search for more papers by this author Author Information Alan Marchant1, Joanna Kargul1,2, Sean T. May1, Philippe Muller3, Alain Delbarre3, Catherine Perrot-Rechenmann3 and Malcolm J. Bennett 1 1Division of Plant Sciences, School of Biological Sciences, University of Nottingham, NG7 2RD UK 2Laboratory of Plant Physiology and Biophysics, Wye College, University of London, Ashford, TN25 5AH UK 3Institut des Sciences Végétales, CNRS, 91198 Gif-sur-Yvette, Cedex, France *Corresponding author. E-mail: [email protected] The EMBO Journal (1999)18:2066-2073https://doi.org/10.1093/emboj/18.8.2066 PDFDownload PDF of article text and main figures. ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinked InMendeleyWechatReddit Figures & Info Plants employ a specialized transport system composed of separate influx and efflux carriers to mobilize the plant hormone auxin between its site(s) of synthesis and action. Mutations within the permease-like AUX1 protein significantly reduce the rate of carrier-mediated auxin uptake within Arabidopsis roots, conferring an agravitropic phenotype. We are able to bypass the defect within auxin uptake and restore the gravitropic root phenotype of aux1 by growing mutant seedlings in the presence of the membrane-permeable synthetic auxin, 1-naphthaleneacetic acid. We illustrate that AUX1 expression overlaps that previously described for the auxin efflux carrier, AtPIN2, using transgenic lines expressing an AUX1 promoter::uidA (GUS) gene. Finally, we demonstrate that AUX1 regulates gravitropic curvature by acting in unison with the auxin efflux carrier to co-ordinate the localized redistribution of auxin within the Arabidopsis root apex. Our results provide the first example of a developmental role for the auxin influx carrier within higher plants and supply new insight into the molecular basis of gravitropic signalling. Introduction Plant hormones influence almost every aspect of plant growth and development (Davis, 1995). Auxins are considered unique amongst plant hormones in demonstrating a polarity in their movement (reviewed by Goldsmith, 1977). Indole-3-acetic acid (IAA), the major form of auxin in higher plants, is first synthesized within young apical tissues, then conveyed to its basal target tissues employing a specialized delivery system termed polar auxin transport (reviewed by Lomax et al., 1995). IAA is transported into and out of the cell across the plasma membrane through the activities of the auxin influx and efflux carriers, respectively. The identification of auxin transport inhibitors such as 1-N-naphthylphthalamic acid (NPA) has greatly facilitated our understanding of the physiological importance of auxin transport (Katekar and Geissler, 1977). Perturbations in gravitropism, lateral root initiation, vascular differentiation and embryonic patterning represent examples of effects reported following treatment of plant tissues with NPA (reviewed by Bennett et al., 1998). All auxin transport inhibitors described to date target the phytotropin binding site within the auxin efflux carrier (reviewed by Lomax et al., 1995). Morris et al. (1991) have proposed that the auxin efflux carrier comprises at least three components: a transmembrane carrier protein, an NPA binding protein and a third, labile regulatory component. Several genes have been identified within the model plant, Arabidopsis thaliana which encode putative auxin efflux carrier components. These genes include the bacterial transporter-like family of EIR/PIN/AGR sequences (Chen et al., 1998; Gälweiler et al., 1998; Luschnig et al., 1998; Müller et al., 1998; Utsuno et al., 1998); TIR3, which encodes (or regulates the activity of) the NPA binding protein based on the reduced rate of polar auxin transport and NPA binding activity of the tir3 mutant (Ruegger et al., 1997); and RCN1, an ortholog of regulatory subunit A of protein phophatase 2A, which represents a putative regulator of efflux carrier activity (Garbers et al., 1996). Many of the morphological changes exhibited by Arabidopsis plants that are mutated in one of the putative efflux carrier components can be phenocopied in wild-type plants following NPA treatment (Okada et al., 1991; Gälweiler et al., 1998), emphasizing the developmental importance of the auxin efflux carrier. Auxin influx carrier activity was first described by Rubery and Sheldrake (1974). Physiologists have questioned the importance of carrier-mediated auxin uptake since the protonated form of IAA is capable of diffusing across plant membranes (Goldsmith, 1977). Determining the developmental importance of carrier-mediated IAA uptake has been hampered by the lack of suitable auxin influx-carrier specific inhibitors (Lomax et al., 1995). Molecular genetic studies within Arabidopsis have led to the identification of the agravitropic mutant, aux1 (Maher and Martindale, 1980). The aux1 mutant of Arabidopsis displays an altered growth response to the auxins IAA or 2,4-dichlorophenoxyacetic acid (2,4-D) (Maher and Martindale, 1980). The AUX1 gene has been cloned and found to encode a highly hydrophobic polypeptide featuring between 10 and 12 transmembrane spanning domains (Bennett et al., 1996). Co-linearity with a family of plant amino acid permeases (Bennett et al., 1996; Fischer et al., 1998) has prompted suggestions that AUX1 performs a transport function, facilitating the uptake of the amino acid-like signalling molecule, IAA. The aux1 mutant therefore provides a promising experimental tool with which to address the function of the auxin influx carrier during Arabidopsis development. We report that mutations within AUX1 impair auxin influx carrier activity. Furthermore, we demonstrate that AUX1 regulates root gravitropism by facilitating auxin uptake within the root apical tissues. Results The aux1 mutant is defective in carrier-mediated auxin uptake We have obtained several lines of evidence indicating that AUX1 regulates auxin uptake carrier activity within Arabidopsis roots. First, mutations within the AUX1 gene selectively confer an altered root growth response towards auxins which require carrier-mediated uptake. Delbarre et al. (1996) have observed previously that the influx carrier facilitates the uptake of IAA and the synthetic auxin 2,4-D, but not the lipophilic auxin, 1-naphthaleneacetic acid (1-NAA), which enters the cell via diffusion (Figure 1A). We have examined whether there was any alteration in the response of aux1 roots towards exogenously applied 2,4-D, IAA and 1-NAA using a root elongation bioassay. Arabidopsis wild-type and aux1 seedlings were germinated in the presence of either 2,4-D, IAA or 1-NAA (Figure 1B, C and D, respectively). All three auxins inhibit wild-type Arabidopsis root elongation at the illustrated concentrations. In contrast, aux1 root growth continues in the presence of either 2,4-D or IAA (Figure 1B and C) but is selectively inhibited by 1-NAA (Figure 1D). A reduced rate of auxin influx within aux1 roots should impair the inhibitory properties of IAA and 2,4-D, but would fail to attenuate the effects of the membrane permeable auxin, 1-NAA. Dose–response curves confirm that aux1 root growth exhibits a wild-type level of sensitivity towards 1-NAA (Figure 1E) but has at least a 10-fold increase in resistance to IAA and 2,4-D compared with the wild-type (Pickett et al. 1990). The selective response of aux1 roots towards IAA and 2,4-D versus 1-NAA is therefore diagnostic of impaired hormone uptake. Figure 1.(A) The auxins IAA, 2,4-D and 1-NAA adopt either carrier-mediated or diffusion-based modes of entry into plant cells, respectively. (B–E) The growth of the aux1 mutant is less sensitive than wild-type to auxins requiring carrier-mediated uptake. Wild-type Arabidopsis (left) and aux1-7 mutant seedlings (right) were germinated on MS agar containing either 10−7M 2,4-D (B), 2×10−7M IAA (C) or 4×10−7M 1-NAA (D) and grown for 5 days in constant white light. (E) Dose–response curve for wild-type (Columbia ecotype) and aux1-7 root elongation in the presence of varying concentrations of 1-NAA (see Materials and methods). Results are expressed as a percentage relative to the growth on hormone-free medium. Bars, 4 mm. Download figure Download PowerPoint We have further tested the auxin influx carrier model for AUX1 function by directly assaying the transport properties of aux1 roots. Root segments from 3- to 5-week-old Arabidopsis plants grown in sterile liquid culture were incubated with radiolabelled auxins. As a substrate for both auxin influx and efflux carriers, IAA exhibits biphasic titration curves when incubated with plant tissues, leading to several reported experimental anomalies including increased levels of apparent IAA uptake in the presence of saturating concentrations of unlabelled IAA (Edwards and Goldsmith, 1980; Morris and Robinson, 1998). In the light of these observations we have used the synthetic auxin 2,4-D since it represents a substrate for the auxin influx carrier alone and therefore exhibits a monophasic titration curve (Delbarre et al., 1996). Short-term auxin accumulation assays were performed in the presence or absence of excess unlabelled 2,4-D in order to measure diffusion versus total uptake, respectively (Figure 2A), and hence calculate the saturable, carrier-mediated uptake value (Figure 2B). The values illustrated within Figure 2 represent data collected from 20 independent uptake experiments using [14C]2,4-D, each performed in triplicate. In summary, wild-type Arabidopsis roots accumulated >2-fold more [14C]2,4-D than aux1 (Figure 2). In contrast, no discernible difference between aux1 and wild-type could be detected when identical uptake experiments were performed using the membrane-diffusible auxin 1-NAA, the IAA-like amino acid tryptophan or the acid-trap control, benzoic acid (data not shown). The selectivity of the transport defect within aux1 roots is therefore consistent with an auxin uptake carrier function for the permease-like protein, AUX1. Figure 2.The saturable uptake of the auxin 2,4-D is reduced in aux1 mutant root cultures. (A) Root fragments from Arabidopsis wild-type and aux1-100 mutant plants were incubated for 5 min with 150 nM [14C]2,4-D. The [14C]2,4-D accumulation ratio represents the ratio of the radioactivity retained per unit weight of root tissue to the radioactivity per unit volume of incubation medium (Materials and methods). Ratios are mean (± SE) of values obtained in 20 independent experiments, each in triplicate. (A) Total and diffusion-based accumulations were measured in the absence or presence of 50 μM unlabelled 2,4-D, respectively. (B) The saturable uptake of the auxin 2,4-D is reduced in aux1 mutant root cultures. The saturable component of [14C]2,4-D accumulation was calculated by subtracting diffusion-based from total accumulation. Download figure Download PowerPoint The diffusible auxin 1-NAA is able to rescue the aux1 agravitropic root phenotype Our results suggest that the aux1 mutant has reduced carrier-mediated auxin uptake activity (Figures 1 and 2). AUX1 could therefore regulate gravitropism by mediating the uptake of auxin into elongating root cells. We rationalize that if AUX1 function is specifically associated with auxin uptake, the membrane permeable auxin, 1-NAA should bypass the aux1 lesion within auxin uptake and restore root gravitropism. We have tested whether 1-NAA could rescue the aux1 agravitropic root phenotype by germinating mutant seedlings on medium containing levels of 1-NAA well below the IC50 for root elongation (Figure 1E). On hormone-free medium, roots of aux1 seedlings grew in a randomized manner (Figure 3A), whereas mutant roots germinated in the presence of 10−7 M 1-NAA grew vertically, exhibiting a positive gravitropic response (Figure 3B). Similarly, 1-NAA was also able to fully restore a root bending response within gravity-stimulated dark grown aux1 seedlings (Figure 3C and D), confirming that 1-NAA rescued gravitropism (rather than phototropism) within mutant roots. The ability of 1-NAA to restore gravitropic root growth within aux1 seedlings exhibited a dose-dependent relationship, in which the direction of aux1 root growth became progressively more randomized at hormone concentrations <10−7 M (data not shown). Figure 3.The lipophilic auxin 1-NAA is able to restore the gravitropic root growth of the aux1 mutant. Mutant aux1-7 seedlings were germinated in the absence (A and C) or presence (B and D) of 10−7M 1-NAA. Seedlings were either grown vertically for 5 days in constant white light (A and B) or placed vertically in white light for 24 h followed by 48 h in the dark, then turned through 90° and grown for a further 24 h in the dark (C and D). Bars, 3 mm. Download figure Download PowerPoint In order to demonstrate the specificity of the effect of 1-NAA on the aux1 mutant phenotype we have performed an identical experiment using the agravitropic auxin-response mutants, axr2 (Wilson et al., 1990) and axr3 (Leyser et al., 1996). Roots of both axr2 and axr3 seedlings appeared plagiotropic when grown in the absence (Figure 4A and C) or presence of 1-NAA (Figure 4B and D). Our inability to bypass the agravitropic defect within the axr3 mutant, for example, is likely to reflect that the AXR3 sequence represents a member of the Aux. IAA gene family (Abel et al., 1995) which encodes nuclear-targeted proteins that are proposed to function as transcription factors (Rouse et al., 1998). Figure 4.(A and D) The agravitropic root growth phenotype of the auxin response mutants axr2 and axr3 cannot be rescued by 1-NAA. The axr2-1 and axr3-1 mutants were germinated on either hormone-free medium (A and C) or medium containing 10−7M 1-NAA (B and D) and grown vertically in constant white light for 5 days. (E and F) The agravitropic root growth phenotype of aux1 can only be partially rescued by 2,4-D. The aux1-7 mutant was germinated on either hormone-free medium (E) or medium containing 2×10−7M 2,4-D (F) and grown vertically in constant white light for 5 days. Bar, 5 mm. Download figure Download PowerPoint The synthetic auxin 2,4-D would not be expected to be as efficient in bypassing the aux1 lesion due to the requirement for its carrier-mediated uptake (Figure 1A). We observed that roots of aux1 seedlings germinated in the presence of 2×10−7 M 2,4-D exhibited reduced root coiling (Figure 4F) in contrast to the seedlings grown on hormone-free medium (Figure 4E). However, the restoration of root gravitropism as obtained with 1-NAA (Figure 3B) was never observed using a similar range of 2,4-D concentrations below its IC50 for root elongation (data not shown). AUX1 is expressed within tissues associated with gravitropic signal transduction The coordinated redistribution of auxin within the root apex has been proposed to regulate root curvature following a gravitropic stimulus (Evans, 1991). We have previously observed that the AUX1 mRNA is localized to the primary root apex using whole-mount in situ hybridization (Bennett et al., 1996). We have performed a more detailed examination of the AUX1 expression pattern within the Arabidopsis primary root in order to pinpoint the specific tissues within which AUX1 functions. A 2.2 kbp AUX1 promoter fragment was fused to the uidA (GUS) reporter gene (Jefferson et al., 1987) and transformed into wild-type Arabidopsis (May et al., 1998). All transgenic lines selected expressed the GUS reporter gene in an identical pattern within Arabidopsis root and shoot meristematic tissues. The spatial expression of the GUS reporter within the primary root apex for one of these transgenic lines, termed LL4, was characterized in greater detail. A longitudinal section through a GUS-stained LL4 root highlights the tissue organization of the Arabidopsis primary root apex (Figure 5). The collection of cuboid-shaped cells at the apex compose the columella tissue which senses changes in root orientation using starch filled plastids termed statoliths (Blancaflor et al., 1998). The root meristem, lying immediately behind the columella tissues, represents the zone of root cell division. The files of cells originating from the meristem demarcate the individual tissues which make up the mature root (Dolan et al., 1993). Each cell progressively enlarges longitudinally as it passes through the zone of elongation. GUS staining can be detected within every tissue of the LL4 root which is distal to its meristem, extending back to the distal and central elongation zones (Figure 5). Closer scrutiny reveals that the meristematic initials, their elongating daughter cells and the lateral root cap stain for GUS activity. In contrast, little or no GUS activity could be detected within the upper three tiers of the gravity-sensing columella cells within the root cap. AUX1 expression is therefore most closely associated with root tissues which transduce and respond to, rather than initially perceive, the gravitropic stimulus. Figure 5.(A) Schematic illustration of root apical tissues delineating root cap (RC), meristematic (M) and elongation zone (EZ). (B) The AUX1 promoter drives GUS reporter gene expression within the majority of tissues within the primary root apex with the exception of the upper three tiers of columella cells within the root cap. Nine-day transgenic Arabidopsis seedlings were stained for GUS activity using conditions designed to minimize diffusion (see Materials and methods), embedded, then sectioned and viewed under bright field. Download figure Download PowerPoint 1-NAA requires auxin efflux carrier activity to rescue aux1 root gravitropism The spatial expression of AUX1 within the epidermal and cortical tissues of the root apex (Figure 5) overlaps with the pattern recently described for the putative auxin efflux carrier component, AtPIN2 (Müller et al., 1998). As a substrate for the auxin efflux carrier (Delbarre et al., 1996), the ability of 1-NAA to rescue the aux1 agravitropic phenotype (Figure 3B and D; Figure 6B) may reflect its capacity to enter root cells by diffusion and be remobilized via the auxin efflux carrier. In order to investigate the requirement for auxin carrier activity to redistribute 1-NAA within root apical tissues following gravistimulation, we have examined whether the efflux carrier inhibitor, NPA, is able to disrupt the ability of 1-NAA to rescue the aux1 agravitropic phenotype. NPA treatment clearly reverses the ability of 1-NAA to rescue aux1 gravitropism (Figure 6D), whereas the addition of NPA alone has little effect on the aux1 agravitropic phenotype (Figure 6C) though the roots tend to be less tightly coiled. Our observations suggest that the ability of 1-NAA to rescue the aux1 agravitropic phenotype reflects its polar movement within root apical tissues through its capacity to enter cells by diffusion and then act as a substrate for auxin efflux carrier activity. Figure 6.NPA is able to block 1-NAA-mediated rescue of the aux1 agravitropic mutant phenotype. Mutant seedlings were germinated on either hormone free medium (A), or medium containing 10−7M 1-NAA (B), 2×10−7M NPA (C) or 2×10−7M NPA and 10−7M 1-NAA (D) and grown for 5 days in constant white light. The orientation of root growth of 50 independent aux1 seedlings was measured after 5 days. Each root was assigned to one of twelve 30° sectors. The length of each bar represents the percentage of seedlings showing direction of root growth within that sector. (A) Roots of untreated aux1 roots remained plagiotropic; whereas (B) 1-NAA treatment completely restores gravitropism, (C) NPA has little effect on the plagiotropic phenotype of aux1 roots, but (D) blocks the ability of 1-NAA to rescue the aux1 gravitropic phenotype. Download figure Download PowerPoint Discussion The permease-like AUX1 polypeptide represents a component of the auxin influx carrier machinery We report several independent lines of evidence which conclude that the AUX1 gene encodes a component of the auxin influx carrier. Auxin accumulation experiments demonstrate that aux1 roots have a significantly reduced capacity to mediate the uptake of the auxin influx carrier substrate, 2,4-D (Figure 2), yet retain a wild-type level of uptake for the membrane permeable auxin 1-NAA. Mutations within AUX1 selectively impair the action of auxins that require carrier-mediated uptake (Figure 1). The selective response of aux1 towards IAA and 2,4-D versus 1-NAA contrasts with that described for other auxin signalling mutants such as axr2 which indiscriminately perturbs responses towards all three hormones (Wilson et al., 1990). Evans et al. (1994) have observed previously that elongating aux1 roots exhibited a significant delay in their response to inhibitory levels of IAA compared to axr2 and wild-type Arabidopsis, prompting the authors to suggest that the aux1 mutant was defective for auxin uptake. The AUX1 gene encodes a highly hydrophobic polypeptide containing 10–12 transmembrane spanning domains whose primary sequence exhibits homology with a family of plant and fungal amino acid transport proteins (Bennett et al., 1996; Fischer et al., 1998). However, aux1 is unlikely to represent an amino acid permease mutation since wild-type and aux1 roots exhibit identical rates of uptake for the indole amino acid tryptophan. AUX1 lacks sequence homology with the recently described family of auxin efflux carrier proteins which appear related to a family of bacterial transporters (Chen et al., 1998; Gälweiler et al., 1998; Luschnig et al., 1998; Müller et al., 1998; Utsuno et al., 1998). Auxin influx and efflux carrier proteins therefore appear to have originated from separate families of transporter sequences. We note that the modified phytohormone response signatures of aux1 and Atpin2 mutants parallel the known substrate specificities of the auxin influx and efflux carriers, respectively (Delbarre et al., 1996). The increased resistance of aux1 roots towards exogenous IAA and 2,4-D contrasts with the elevated sensitivity of Atpin2 roots towards 1-NAA (Chen et al., 1998; Müller et al., 1998). Mutations within AUX1 and AtPIN2 also confer elevated resistance towards the plant hormone ethylene and its precursor, 1-aminocyclopropane-1-carboxylic acid (ACC) (Pickett et al., 1990; Chen et al., 1998; Luschnig et al., 1998; Müller et al., 1998). Epistasis experiments indicate that AUX1 and AtPIN2 (EIR1) act downstream of the ethylene receptor ETR1 and its signal transduction component, EIN2 (Roman et al., 1995). Ethylene has been demonstrated to influence polar auxin transport within etiolated pea epicotyls by down-regulating auxin efflux carrier activity (Suttle, 1988). Such observations suggest that ethylene mediates many of its growth regulatory effects by acting as a global regulator of the auxin transport machinery. Root gravitropism requires auxin influx carrier activity Auxin transport plays an important role during root gravitropism. Earlier workers have demonstrated that roots treated with inhibitors which block auxin efflux carrier activity disrupt gravitropism (reviewed by Lomax et al., 1995). Results presented in this study highlight the importance of auxin influx carrier activity for root gravitropism. We have demonstrated that roots of the aux1 mutant have impaired carrier-mediated auxin uptake activity (Figures 1 and 2). Artificially elevating the rate of phytohormone uptake into plant cells by growing mutant seedlings in the presence of the membrane-diffusible auxin 1-NAA restores root gravitropism (Figure 3). In contrast, the less diffusible auxin 2,4-D only partially restores root gravitopism (Figure 4). We conclude that the reduced rate of auxin uptake into root apical cells represents the physiological basis for the agravitropic root phenotype of the aux1 mutant. Moreover, the response of aux1 roots towards 1-NAA (Figures 1 and 3) suggests that the auxin signalling machinery within the aux1 root is essentially intact and that the biochemical defect is limited to the auxin uptake machinery. This contrasts with the agravitropic phenotype of the mutant axr3 which cannot be bypassed by 1-NAA (Figure 4), in agreement with its genetic lesion disrupting a later step within the auxin signalling pathway (Rouse et al., 1998). Root gravitropism requires local auxin transport mediated by auxin influx and efflux carrier components AUX1 and AtPIN2 Microautoradiographic studies have highlighted the presence of two separate auxin transport streams within roots (Tsurumi and Ohwaki, 1978). The polar auxin transport stream mediates basipetal, long distance movement of IAA from its apical site(s) of synthesis, whereas during local auxin transport within the root apex IAA is redistributed acropetally amongst the rapidly dividing and growing cells of the meristematic and elongation zones, respectively (Figure 7). Components from both auxin transport streams have recently been identified (Bennett et al., 1996; Chen et al., 1998; Gälweiler et al., 1998; Luschnig et al., 1998; Müller et al., 1998; Utsuno et al., 1998). These studies have concluded that AUX1 and AtPIN2 are expressed within root apical tissues mediating local auxin transport (Figure 5; Müller et al., 1998), whereas AtPIN1 is localized within vascular tissues associated with polar auxin transport (Gälweiler et al., 1998). Until these recent studies, the relative importance of local versus polar auxin transport in root gravitropism had been unclear since phytotropins such as NPA block both auxin transport pathways. Molecular genetic studies have now demonstrated that mutations within AUX1 and AtPIN2 (but not AtPIN1) cause agravitropic root phenotypes (this study; Chen et al., 1998; Gälweiler et al., 1998; Luschnig et al., 1998; Müller et al., 1998; Utsuno et al., 1998), indicating that local auxin transport is of primary importance to root gravitropism. Figure 7.Contrasting models for the role of auxin transport during root gravitropism featuring either facilitative (A) or regulatory (B) modes of action for auxin. The (upper) single, large arrow signifies polar auxin transport whereas the (lower) bifurcated arrow represents local auxin transport mediating hormone redistribution within root apical tissues. Download figure Download PowerPoint We have presented evidence that auxin influx and efflux carriers act in unison to coordinate the localized redistribution of IAA within root apical cells (Figure 6). Our model is supported by the observation that auxin influx and efflux carrier components AUX1 and AtPIN2 are expressed in an overlapping pattern within root apical tissues (Figure 5; Müller et al., 1998). The AUX1 transcript is expressed within all root apical tissues from the root cap to the distal/central elongation zone with the exception of the upper three tiers of the columella tissues (Figure 5). The AtPIN2 protein has been immunolocalized within epidermal and cortical cells of the distal/central elongation zone (Müller et al., 1998) which represents a subset of the tissues expressing the GUS transgene under the control of the AUX1 promoter (Figure 5). Significantly, the AtPIN2 protein has been immunolocalized to the basal end of elongating root cells (Müller et al., 1998), prompting suggestions that its asymme" @default.
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• W2024692287 title "AUX1 regulates root gravitropism in Arabidopsis by facilitating auxin uptake within root apical tissues" @default.
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