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• W2808068377 abstract "Recent findings in active auxin transport over organelle membranes and the influence of apoplastic and cytosolic pH on passive auxin flow into the cell highlight the importance of short-distance auxin transport for local auxin maxima in roots exposed to stress. Based on previously published gene expression data, we have identified stress-induced expression patterns of IAA biosynthesis and conjugation genes in the root that could be relevant for IAA accumulation patterns. These results underscore the importance of incorporating IAA homeostasis into models predicting auxin levels and flow. Recent advances in mathematical models involving auxin-related processes highlight the value of combining in planta and in silico experiments when unraveling complex hormonal changes in plants. In most abiotic stress conditions, including salinity and water deficit, the developmental plasticity of the plant root is regulated by the phytohormone auxin. Changes in auxin concentration are often attributed to changes in shoot-derived long-distance auxin flow. However, recent evidence suggests important contributions by short-distance auxin transport from local storage and local auxin biosynthesis, conjugation, and oxidation during abiotic stress. We discuss here current knowledge on long-distance auxin transport in stress responses, and subsequently debate how short-distance auxin transport and indole-3-acetic acid (IAA) metabolism play a role in influencing eventual auxin accumulation and signaling patterns. Our analysis stresses the importance of considering all these components together and highlights the use of mathematical modeling for predictions of plant physiological responses. In most abiotic stress conditions, including salinity and water deficit, the developmental plasticity of the plant root is regulated by the phytohormone auxin. Changes in auxin concentration are often attributed to changes in shoot-derived long-distance auxin flow. However, recent evidence suggests important contributions by short-distance auxin transport from local storage and local auxin biosynthesis, conjugation, and oxidation during abiotic stress. We discuss here current knowledge on long-distance auxin transport in stress responses, and subsequently debate how short-distance auxin transport and indole-3-acetic acid (IAA) metabolism play a role in influencing eventual auxin accumulation and signaling patterns. Our analysis stresses the importance of considering all these components together and highlights the use of mathematical modeling for predictions of plant physiological responses. Drought and increasing salinity are abiotic stresses that cause major decreases in crop yield worldwide. Drought causes loss of crops through water deficit, whereas increasing soil salinity induces osmotic and ionic stress in the plants. Both abiotic stresses are a threat to the amount of arable land that is fit for our food production. Although the development of crops tolerant to these conditions has received attention [1Mickelbart M.V. et al.Genetic mechanisms of abiotic stress tolerance that translate to crop yield stability.Nat. Rev. Genet. 2015; 16: 237-251Crossref PubMed Scopus (571) Google Scholar], a greater research focus has been on generating biotic stress resistance and increasing the yield of edible parts of the plant. Now that we face a rapid deterioration of arable land, research on the tolerance to abiotic stresses has substantially increased. Phenotypic plasticity, including developmental modifications to root system architecture (RSA), is vital for tolerance to water deficiency and high soil salinity. RSA and root growth rates during plant development under optimal conditions have been well studied, and it has long been established that these require the phytohormone auxin (see Glossary). Recently our fundamental understanding of root developmental plasticity during abiotic stress has markedly improved [2Koevoets I.T. et al.Roots withstanding their environment: exploiting root system architecture responses to abiotic stress to improve crop tolerance.Front. Plant Sci. 2016; 7: 1335Crossref PubMed Scopus (256) Google Scholar]. Unsurprisingly, auxin plays an important role during abiotic stress-induced changes in the root. Through the creation of local auxin maxima, cell elongation is locally inhibited and the emergence of lateral roots can be arrested. On the other hand, local auxin minima were found to be a signal that triggers the transition from cell division to cell differentiation in roots of arabidopsis (Arabidopsis thaliana) [3Di Mambro R. et al.Auxin minimum triggers the developmental switch from cell division to cell differentiation in the Arabidopsis root.Proc. Natl. Acad. Sci. U. S. A. 2017; 114: E7641-E7649Crossref PubMed Scopus (145) Google Scholar]. The different processes that together determine auxin-mediated regulation of growth and development during abiotic stress are auxin transport, biosynthesis, conjugation, perception, and signaling. Auxin transport has received much attention, and the role of polar auxin transport (PAT) by auxin carrier proteins during unstressed conditions and gravitropism has been well established [4Adamowski M. Friml J. PIN-dependent auxin transport: action, regulation, and evolution.Plant Cell. 2015; 27: 20-32Crossref PubMed Scopus (460) Google Scholar, 5Naramoto S. Polar transport in plants mediated by membrane transporters: focus on mechanisms of polar auxin transport.Curr. Opin. Plant Biol. 2017; 40: 8-14Crossref PubMed Scopus (62) Google Scholar, 6Armengot L. et al.Regulation of polar auxin transport by protein and lipid kinases.J. Exp. Bot. 2016; 67: 4015-4037Crossref PubMed Scopus (83) Google Scholar]. By contrast, the changes in PAT during abiotic stresses remain largely unknown. How changes in local auxin biosynthesis and IAA conjugation during abiotic stress affect root responses is another relatively young field of research. The integration of all these different aspects of auxin homeostasis is complicated because the many factors involved all influence each other and there is extensive crosstalk between auxin and other hormones. One promising solution to this problem is the rapidly emerging field of computational modeling of auxin processes in the plant root. The main mechanism to maintain the ‘upside-down fountain’ of auxin flow in the root is PAT. Clarification of the role of long-distance shoot-derived auxin transport in abiotic stress has advanced our understanding of the changes in auxin carrier proteins and other proteins that influence auxin flow in the root (Figure 1). Internalization of the auxin efflux carrier PIN-formed 2 (PIN2) either during halotropism on the side of the root facing a higher salt concentration [7Galvan-Ampudia C.S. et al.Halotropism is a response of plant roots to avoid a saline environment.Curr. Biol. 2013; 23: 2044-2050Abstract Full Text Full Text PDF PubMed Scopus (201) Google Scholar] or during osmotic stress treatments [8Zwiewka M. et al.Osmotic stress modulates the balance between exocytosis and clathrin-mediated endocytosis in Arabidopsis thaliana.Mol. Plant. 2015; 8: 1175-1187Abstract Full Text Full Text PDF PubMed Scopus (75) Google Scholar] has been shown. Subsequently, by combining in planta salt stress experiments with computational modeling, it was concluded that internalization of PIN2 is not sufficient to explain the alteration of auxin flow during halotropism [9van den Berg T. et al.Modeling halotropism: a key role for root tip architecture and reflux loop remodeling in redistributing auxin.Development. 2016; 143: 3350-3362Crossref PubMed Scopus (45) Google Scholar], and changes in PIN-formed 1 (PIN1) and auxin transporter protein 1 (AUX1) were shown to co-facilitate the fast change of auxin flow. In addition to root growth, auxin efflux carriers are suggested to regulate meristem size during salt stress [10Liu W. et al.Salt stress reduces root meristem size by nitric oxide-mediated modulation of auxin accumulation and signaling in Arabidopsis.Plant Physiol. 2015; 168: 343-356Crossref PubMed Scopus (226) Google Scholar]. Reduced PIN1, PIN3, and PIN7 expression and auxin-resistant 3 (AXR3)/indole-3-acetic acid 17 (IAA17) stabilization during salt stress have been proposed to influence the root meristem size by increasing nitric oxide (NO) levels. Another large family of auxin carriers influencing auxin flow in the root is the ABCB transporter family [11Geisler M. et al.A critical view on ABC transporters and their interacting partners in auxin transport.Plant Cell Physiol. 2017; 58: 1601-1614Crossref PubMed Scopus (79) Google Scholar]. Recently, several studies have shown a role for ABCB transporters during salt stress. Of 22 different ABCB transporters in rice (Oryza sativum), the expression of 21 was found to change in response to salinity and drought [12Chai C. Subudhi P.K. Comprehensive analysis and expression profiling of the OsLAX and OsABCB auxin transporter gene families in rice (Oryza sativa) under phytohormone stimuli and abiotic stresses.Front. Plant Sci. 2016; 7: 593Crossref PubMed Scopus (27) Google Scholar, 13Han E.H. et al.‘Bending’ models of halotropism: incorporating protein phosphatase 2A, ABCB transporters, and auxin metabolism.J. Exp. Bot. 2017; 68: 3071-3089Crossref PubMed Scopus (17) Google Scholar]. Of the root-expressed ABCB auxin transporters, the expression of ABCB1 and 19 was slightly upregulated, whereas ABCB4 showed downregulation after 1 h of salt stress. Reduced acropetal transport of auxin was observed in an abcb19 null mutant, whereas basipetal transport was unaltered [14Cho M. et al.Block of ATP-binding cassette B19 ion channel activity by 5-nitro-2-(3-phenylpropylamino)-benzoic acid impairs polar auxin transport and root gravitropism.Plant Physiol. 2014; 166: 2091-2099Crossref PubMed Scopus (17) Google Scholar]. Other genes, whose loss-of-function mutants were recently observed to exhibit altered auxin flow in the root, are putatively involved in abiotic stress tolerance. Mutants of interactor of synaptotagmin 1 (ROSY1-1) showed a decrease in basipetal auxin transport and exhibited increased salt tolerance, which was ascribed to the interaction between ROSY1-1 and synaptotagmin 1 (SYT1) [15Dalal J. et al.ROSY1, a novel regulator of gravitropic response is a stigmasterol binding protein.J. Plant Physiol. 2016; 196/197: 28-40Crossref Scopus (25) Google Scholar]. Furthermore, zinc-induced facilitator-like 1 (ZIFL1), a major facilitator superfamily (MFS) transporter, regulates shootward auxin efflux in the root [16Remy E. et al.A major facilitator superfamily transporter plays a dual role in polar auxin transport and drought stress tolerance in Arabidopsis.Plant Cell. 2013; 25: 901-926Crossref PubMed Scopus (146) Google Scholar]. zifl1 loss-of-function mutants were observed to have reduced PIN2 protein abundance in epidermal root cells after external application of IAA and had gravitropic bending defects. Changes in auxin transport between different intracellular compartments also influence the auxin that is available for the formation of local auxin maxima. Auxin located in the acidic vacuole, with a pH of 5.0 to 5.5, will tend to move towards the cytosol which has a pH of ∼7. During salt stress the cytosolic pH drops [17Gao D. et al.Self-reporting Arabidopsis expressing pH and [Ca2+] indicators unveil ion dynamics in the cytoplasm and in the apoplast under abiotic stress.Plant Physiol. 2004; 134: 898-908Crossref PubMed Scopus (160) Google Scholar], thus theoretically reducing passive auxin efflux from the vacuole. Apoplastic pH is also suggested to be involved in passive auxin influx into the cells (Box 1).Box 1Apoplastic pH and Auxin MovementAuxin transport is, in addition to active processes, dependent on passive movement of IAA into or between cells and movement through the apoplast. The concentration of auxin influences apoplastic pH, which in turn influences passive auxin transport into cells. In roots, high cellular auxin concentrations inhibit cell elongation, whereas in the shoot, in accordance with the acid growth theory, auxin causes cell elongation [66Rayle D.L. Cleland R. Enhancement of wall loosening and elongation by acid solutions.Plant Physiol. 1970; 46: 250-253Crossref PubMed Google Scholar, 67Rayle D.L. Cleland R.E. The acid growth theory of auxin-induced cell elongation is alive and well.Plant Physiol. 1992; 99: 1271-1274Crossref PubMed Scopus (629) Google Scholar].The effect of auxin on apoplastic pH has been demonstrated by the addition of exogenous auxin to arabidopsis roots, which induced fast alkalization of the apoplast [68Barbez E. et al.Auxin steers root cell expansion via apoplastic pH regulation in Arabidopsis thaliana.Proc. Natl. Acad. Sci. U. S. A. 2017; 114: E4884-E4893Crossref PubMed Scopus (170) Google Scholar]. However, after prolonged exposure (8 h) the root apoplast becomes acidified. Similarly, initial alkalization of the apoplast followed by acidification after 19 h was found when endogenous auxin levels were elevated by induced expression of YUCCA6 [68Barbez E. et al.Auxin steers root cell expansion via apoplastic pH regulation in Arabidopsis thaliana.Proc. Natl. Acad. Sci. U. S. A. 2017; 114: E4884-E4893Crossref PubMed Scopus (170) Google Scholar]. Barbez and colleagues have demonstrated that cell-wall acidification triggers cell elongation in arabidopsis seedlings. Their data imply that endogenous auxin concentrations regulate apoplast acidification, which in turn regulates cell elongation. During exposure of roots to a salt gradient, auxin redistributes in the root [7Galvan-Ampudia C.S. et al.Halotropism is a response of plant roots to avoid a saline environment.Curr. Biol. 2013; 23: 2044-2050Abstract Full Text Full Text PDF PubMed Scopus (201) Google Scholar, 69Wang Y. et al.Auxin redistribution modulates plastic development of root system architecture under salt stress in Arabidopsis thaliana.J. Plant Physiol. 2009; 166: 1637-1645Crossref PubMed Scopus (147) Google Scholar], suggesting that local alterations in apoplastic pH levels during salt stress might influence cell elongation. In addition, following 1 h root exposure to NaCl a transient increase in apoplastic pH was observed [17Gao D. et al.Self-reporting Arabidopsis expressing pH and [Ca2+] indicators unveil ion dynamics in the cytoplasm and in the apoplast under abiotic stress.Plant Physiol. 2004; 134: 898-908Crossref PubMed Scopus (160) Google Scholar]. Following a 100 mM NaCl pulse apoplastic pH returned to control levels 1 h after the transient increase in apoplastic pH. The cytoplasmic pH decreased slightly upon NaCl exposure but did not recover. The changes in passive auxin transport as a result of this alteration in apoplast pH have not yet been studied in vivo. Nonetheless, a mathematical/computational model linking auxin and pH dynamics has been created [61Steinacher A. et al.A computational model of auxin and pH dynamics in a single plant cell.J. Theor. Biol. 2012; 296: 84-94Crossref PubMed Scopus (28) Google Scholar]. The main conclusions from this model are that long-term auxin-induced apoplast acidification leads to increased auxin transport across the plasma membrane and significantly higher auxin concentrations in the cytoplasm. However, it has also been reported that the level of passive auxin influx would be negligible at low apoplastic pH (<5.7) in protoplasts [70Rutschow H.L. et al.The carrier AUXIN RESISTANT (AUX1) dominates auxin flux into Arabidopsis protoplasts.New Phytol. 2014; 204: 536-544Crossref PubMed Scopus (23) Google Scholar]. This would mean that all changes in intracellular auxin levels take place through active auxin transport, and there is no role for passive auxin transport in pH-induced alteration of cell elongation during abiotic stress. In vivo measurements of cellular auxin influx and efflux during apoplast acidification will be necessary to elucidate the role of passive auxin transport across the plasma membrane. Auxin transport is, in addition to active processes, dependent on passive movement of IAA into or between cells and movement through the apoplast. The concentration of auxin influences apoplastic pH, which in turn influences passive auxin transport into cells. In roots, high cellular auxin concentrations inhibit cell elongation, whereas in the shoot, in accordance with the acid growth theory, auxin causes cell elongation [66Rayle D.L. Cleland R. Enhancement of wall loosening and elongation by acid solutions.Plant Physiol. 1970; 46: 250-253Crossref PubMed Google Scholar, 67Rayle D.L. Cleland R.E. The acid growth theory of auxin-induced cell elongation is alive and well.Plant Physiol. 1992; 99: 1271-1274Crossref PubMed Scopus (629) Google Scholar]. The effect of auxin on apoplastic pH has been demonstrated by the addition of exogenous auxin to arabidopsis roots, which induced fast alkalization of the apoplast [68Barbez E. et al.Auxin steers root cell expansion via apoplastic pH regulation in Arabidopsis thaliana.Proc. Natl. Acad. Sci. U. S. A. 2017; 114: E4884-E4893Crossref PubMed Scopus (170) Google Scholar]. However, after prolonged exposure (8 h) the root apoplast becomes acidified. Similarly, initial alkalization of the apoplast followed by acidification after 19 h was found when endogenous auxin levels were elevated by induced expression of YUCCA6 [68Barbez E. et al.Auxin steers root cell expansion via apoplastic pH regulation in Arabidopsis thaliana.Proc. Natl. Acad. Sci. U. S. A. 2017; 114: E4884-E4893Crossref PubMed Scopus (170) Google Scholar]. Barbez and colleagues have demonstrated that cell-wall acidification triggers cell elongation in arabidopsis seedlings. Their data imply that endogenous auxin concentrations regulate apoplast acidification, which in turn regulates cell elongation. During exposure of roots to a salt gradient, auxin redistributes in the root [7Galvan-Ampudia C.S. et al.Halotropism is a response of plant roots to avoid a saline environment.Curr. Biol. 2013; 23: 2044-2050Abstract Full Text Full Text PDF PubMed Scopus (201) Google Scholar, 69Wang Y. et al.Auxin redistribution modulates plastic development of root system architecture under salt stress in Arabidopsis thaliana.J. Plant Physiol. 2009; 166: 1637-1645Crossref PubMed Scopus (147) Google Scholar], suggesting that local alterations in apoplastic pH levels during salt stress might influence cell elongation. In addition, following 1 h root exposure to NaCl a transient increase in apoplastic pH was observed [17Gao D. et al.Self-reporting Arabidopsis expressing pH and [Ca2+] indicators unveil ion dynamics in the cytoplasm and in the apoplast under abiotic stress.Plant Physiol. 2004; 134: 898-908Crossref PubMed Scopus (160) Google Scholar]. Following a 100 mM NaCl pulse apoplastic pH returned to control levels 1 h after the transient increase in apoplastic pH. The cytoplasmic pH decreased slightly upon NaCl exposure but did not recover. The changes in passive auxin transport as a result of this alteration in apoplast pH have not yet been studied in vivo. Nonetheless, a mathematical/computational model linking auxin and pH dynamics has been created [61Steinacher A. et al.A computational model of auxin and pH dynamics in a single plant cell.J. Theor. Biol. 2012; 296: 84-94Crossref PubMed Scopus (28) Google Scholar]. The main conclusions from this model are that long-term auxin-induced apoplast acidification leads to increased auxin transport across the plasma membrane and significantly higher auxin concentrations in the cytoplasm. However, it has also been reported that the level of passive auxin influx would be negligible at low apoplastic pH (<5.7) in protoplasts [70Rutschow H.L. et al.The carrier AUXIN RESISTANT (AUX1) dominates auxin flux into Arabidopsis protoplasts.New Phytol. 2014; 204: 536-544Crossref PubMed Scopus (23) Google Scholar]. This would mean that all changes in intracellular auxin levels take place through active auxin transport, and there is no role for passive auxin transport in pH-induced alteration of cell elongation during abiotic stress. In vivo measurements of cellular auxin influx and efflux during apoplast acidification will be necessary to elucidate the role of passive auxin transport across the plasma membrane. Isolated vacuoles from protoplasts lacking the tonoplast-located auxin carrier WAT1 (walls are thin 1) were found to accumulate significantly more radiolabeled auxin than wild-type vacuoles, indicating active transport of auxin from the vacuole to the cytoplasm by WAT1 [18Ranocha P. et al.Arabidopsis WAT1 is a vacuolar auxin transport facilitator required for auxin homoeostasis.Nat. Commun. 2013; 42625Crossref PubMed Scopus (181) Google Scholar]. Recently, an auxin transport facilitator family, located on the endoplasmic reticulum (ER), was identified. PIN-LIKES (PILS) proteins are believed to be involved in auxin homeostasis through auxin accumulation at the ER, in this way limiting the IAA available for nuclear auxin signaling. The change in available IAA alters the cellular sensitivity to auxin. Increased auxin export from pils2/pils5 protoplast cells was also observed [19Barbez E. et al.A novel putative auxin carrier family regulates intracellular auxin homeostasis in plants.Nature. 2012; 485: 119-122Crossref PubMed Scopus (268) Google Scholar]. In addition, a pils2 arabidopsis mutant, and even more so a pils2/pils5 double mutant, showed significantly longer roots than the wild type and a higher lateral root density, suggesting PILS involvement in auxin-dependent root growth. Other forms of passive auxin transport include movement without the interference of membranes. IAA is a small molecule and is therefore able to move freely through the plasmodesmata (PD) in its ionized form (IAA−). To restrict free cell-to-cell movement of IAA during auxin gradient formation, GLUCAN SYNTHASE-LIKE 8 (GSL8) induces an increase of plasmodesma-localized callose. This reduces the symplasmic permeability to maintain local auxin maxima [20Han X. et al.Auxin–callose-mediated plasmodesmal gating is essential for tropic auxin gradient formation and signaling.Dev. Cell. 2014; 28: 132-146Abstract Full Text Full Text PDF PubMed Scopus (122) Google Scholar]. GSL8 expression was found to be upregulated by adding exogenous IAA. Although these results demonstrate the importance of local auxin movement, the relation to abiotic stress remains to be elucidated. In addition to transport, auxin (IAA) levels are determined by biosynthesis and conjugation. Both processes have recently shown to be affected by abiotic stress in the root. Although several IAA biosynthesis pathways has been described [21Di D.-W. et al.The biosynthesis of auxin: how many paths truly lead to IAA?.Plant Growth Regul. 2015; 78: 275-285Crossref Scopus (67) Google Scholar, 22Tivendale N.D. et al.The shifting paradigms of auxin biosynthesis.Trends Plant Sci. 2014; 19: 44-51Abstract Full Text Full Text PDF PubMed Scopus (111) Google Scholar], the indole-3-pyruvic acid (IPyA) pathway is considered to be responsible for most IAA biosynthesis in higher plants [23Mashiguchi K. et al.The main auxin biosynthesis pathway in Arabidopsis.Proc. Natl. Acad. Sci. U. S. A. 2011; 108: 18512-18517Crossref PubMed Scopus (629) Google Scholar, 24Won C. et al.Conversion of tryptophan to indole-3-acetic acid by TRYPTOPHAN AMINOTRANSFERASES OF ARABIDOPSIS and YUCCAs in Arabidopsis.Proc. Natl. Acad. Sci. U. S. A. 2011; 108: 18518-18523Crossref PubMed Scopus (437) Google Scholar]. In addition, for the Brassicaceae family, the indole-3-acetaldoxime (IAOx) pathway has been increasingly identified to play a role during several stress responses [25Julkowska M.M. et al.Genetic components of root architecture remodeling in response to salt stress.Plant Cell. 2017; 29: 3198-3213Crossref PubMed Scopus (86) Google Scholar, 26Lehmann T. et al.Arabidopsis NITRILASE 1 contributes to the regulation of root growth and development through modulation of auxin biosynthesis in seedlings.Front. Plant Sci. 2017; 8: 36Crossref PubMed Scopus (39) Google Scholar, 27Zhao Y. et al.Trp-dependent auxin biosynthesis in Arabidopsis: involvement of cytochrome P450s CYP79B2 and CYP79B3.Genome Res. 2002; 16: 3100-3112Google Scholar], whereas the significance of the other pathways remains under debate and needs further research [21Di D.-W. et al.The biosynthesis of auxin: how many paths truly lead to IAA?.Plant Growth Regul. 2015; 78: 275-285Crossref Scopus (67) Google Scholar, 22Tivendale N.D. et al.The shifting paradigms of auxin biosynthesis.Trends Plant Sci. 2014; 19: 44-51Abstract Full Text Full Text PDF PubMed Scopus (111) Google Scholar]. We focus here on the IPyA and IAOx pathways, and on how these pathways are modulated during abiotic stress. The IPyA pathway (Figure 1) generates IAA via a two-step conversion from tryptophan, with IPyA as the intermediate [27Zhao Y. et al.Trp-dependent auxin biosynthesis in Arabidopsis: involvement of cytochrome P450s CYP79B2 and CYP79B3.Genome Res. 2002; 16: 3100-3112Google Scholar, 28Stepanova A.N. et al.TAA1-mediated auxin biosynthesis is essential for hormone crosstalk and plant development.Cell. 2008; 133: 177-191Abstract Full Text Full Text PDF PubMed Scopus (793) Google Scholar, 29Tao Y. et al.Rapid synthesis of auxin via a new tryptophan-dependent pathway is required for shade avoidance in plants.Cell. 2008; 133: 164-176Abstract Full Text Full Text PDF PubMed Scopus (753) Google Scholar]. The family of YUCCA proteins governs the second step of the pathway [27Zhao Y. et al.Trp-dependent auxin biosynthesis in Arabidopsis: involvement of cytochrome P450s CYP79B2 and CYP79B3.Genome Res. 2002; 16: 3100-3112Google Scholar]. Eleven YUCCA isoforms have been described in arabidopsis, and specific roles for several YUCCAs are slowly being elucidated. The YUCCAs can be divided into mainly root- or shoot-active proteins [30Chen Q. et al.Auxin overproduction in shoots cannot rescue auxin deficiencies in Arabidopsis roots.Plant Cell Physiol. 2014; 55: 1072-1079Crossref PubMed Scopus (142) Google Scholar, 31Cheng Y. et al.Auxin biosynthesis by the YUCCA flavin monooxygenases controls the formation of floral organs and vascular tissues in Arabidopsis.Genes Dev. 2006; 20: 1790-1799Crossref PubMed Scopus (808) Google Scholar]. YUC3, 5, 7, 8, and 9 display distinct expression patterns in the root, whereas other YUCCAs show minor or no expression in the root [30Chen Q. et al.Auxin overproduction in shoots cannot rescue auxin deficiencies in Arabidopsis roots.Plant Cell Physiol. 2014; 55: 1072-1079Crossref PubMed Scopus (142) Google Scholar]. This illustrates the specificity of different genes in this pathway for specific developmental processes. Although little research on the specificity of YUCCAs for different stresses has been carried out, several gene expression studies do indicate this specificity. For example, YUC2, 5, 8, and 9 show upregulation in plants experiencing shade [32Li L. et al.Linking photoreceptor excitation to changes in plant architecture.Genes Dev. 2012; 26: 785-790Crossref PubMed Scopus (348) Google Scholar], and knockout mutants of these quadruple YUCCA lack shade-induced hypocotyl elongation [33Nozue K. et al.Shade avoidance components and pathways in adult plants revealed by phenotypic profiling.PLoS Genet. 2015; 11e1004953Crossref PubMed Scopus (60) Google Scholar]. Several papers show that overexpression of the IPyA pathway leads to increased salt tolerance in several species [34Ke Q. et al.Transgenic poplar expressing Arabidopsis YUCCA6 exhibits auxin-overproduction phenotypes and increased tolerance to abiotic stress.Plant Physiol. Biochem. 2015; 94: 19-27Crossref PubMed Scopus (81) Google Scholar, 35Kim J.I. et al.Overexpression of Arabidopsis YUCCA6 in potato results in high-auxin developmental phenotypes and enhanced resistance to water deficit.Mol. Plant. 2013; 6: 337-349Abstract Full Text Full Text PDF PubMed Scopus (130) Google Scholar, 36Yan S. et al.Different cucumber CsYUC genes regulate response to abiotic stresses and flower development.Sci. Rep. 2016; 620760Crossref PubMed Scopus (34) Google Scholar]. For example, it was shown in cucumber that specific YUCCAs are expressed at high and low temperature and in response to salinity [36Yan S. et al.Different cucumber CsYUC genes regulate response to abiotic stresses and flower development.Sci. Rep. 2016; 620760Crossref PubMed Scopus (34) Google Scholar]. In salinity, CsYUC10b is strongly upregulated and CsYUC10a and CsYUC11 are strongly downregulated, whereas overexpression of CsYUC11 leads to higher salinity tolerance [36Yan S. et al.Different cucumber CsYUC genes regulate response to abiotic stresses and flower development.Sci. Rep. 2016; 620760Crossref PubMed Scopus (34) Google Scholar]. For arabidopsis, the role of specific YUCCAs during salt stress is so far unknown. Analysis of previously published microarray data [37Dinneny J.R. et al.Cell identity mediates the response of Arabidopsis roots to abiotic stress.Science. 2008; 320: 942-945Crossref PubMed Scopus (567) Google Scholar, 38Kilian J. et al.The AtGenExpress global stress expression data set: protocols, evaluation and model data analysis of UV-B light, drought and cold stress responses.Plant J. 2007; 50: 347-363Crossref PubMed Scopus (1076) Google Scholar] confirms the root specificity of YUC3, 5, 8, and 9 (Table S1 in the supplemental information online). Furthermore, tissue-specific microarray data indicate a shift from strong expression of YUCCAs in columnella under control conditions to strong expression in the epidermis and cortex during salt stress (Figures 1, 2A, and Table S1). Because expression of YUCCAs is low in the epidermis and cortex under control conditions, and thus auxin levels in these cells would mainly depend on transport, this is an interesting shift. Salt stress also has m" @default.
• W2808068377 created "2018-06-21" @default.
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• W2808068377 date "2018-09-01" @default.
• W2808068377 modified "2023-10-18" @default.
• W2808068377 title "Out of Shape During Stress: A Key Role for Auxin" @default.
• W2808068377 cites W1598433638 @default.
• W2808068377 cites W1826179259 @default.
• W2808068377 cites W1965651398 @default.
• W2808068377 cites W1973504406 @default.
• W2808068377 cites W1975130438 @default.
• W2808068377 cites W1975426237 @default.
• W2808068377 cites W1983743834 @default.
• W2808068377 cites W1984846906 @default.
• W2808068377 cites W1985630455 @default.
• W2808068377 cites W1988526541 @default.
• W2808068377 cites W1993924390 @default.
• W2808068377 cites W1994470158 @default.
• W2808068377 cites W1996440573 @default.
• W2808068377 cites W2000319772 @default.
• W2808068377 cites W2004979058 @default.
• W2808068377 cites W2008758248 @default.
• W2808068377 cites W2016940213 @default.
• W2808068377 cites W2018051749 @default.
• W2808068377 cites W2029548988 @default.
• W2808068377 cites W2030020375 @default.
• W2808068377 cites W2039064403 @default.
• W2808068377 cites W2052315279 @default.
• W2808068377 cites W2070052076 @default.
• W2808068377 cites W2074653915 @default.
• W2808068377 cites W2086654822 @default.
• W2808068377 cites W2090769787 @default.
• W2808068377 cites W2091868541 @default.
• W2808068377 cites W2097923768 @default.
• W2808068377 cites W2109354542 @default.
• W2808068377 cites W2125217159 @default.
• W2808068377 cites W2126197960 @default.
• W2808068377 cites W2126623160 @default.
• W2808068377 cites W2129073060 @default.
• W2808068377 cites W2136136435 @default.
• W2808068377 cites W2136440184 @default.
• W2808068377 cites W2139364461 @default.
• W2808068377 cites W2142524542 @default.
• W2808068377 cites W2150943030 @default.
• W2808068377 cites W2152002853 @default.
• W2808068377 cites W2157358805 @default.
• W2808068377 cites W2158957969 @default.
• W2808068377 cites W2162808103 @default.
• W2808068377 cites W2166878800 @default.
• W2808068377 cites W2169918138 @default.
• W2808068377 cites W2170109671 @default.
• W2808068377 cites W2171029961 @default.
• W2808068377 cites W2183404301 @default.
• W2808068377 cites W2274539775 @default.
• W2808068377 cites W2306935015 @default.
• W2808068377 cites W2346585004 @default.
• W2808068377 cites W2418508998 @default.
• W2808068377 cites W2487257704 @default.
• W2808068377 cites W2511053189 @default.
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• W2808068377 cites W2596409380 @default.
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• W2808068377 cites W2725014529 @default.
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• W2808068377 cites W2740713512 @default.
• W2808068377 cites W2742965584 @default.
• W2808068377 cites W2745820147 @default.
• W2808068377 cites W2750516380 @default.
• W2808068377 cites W2767212984 @default.
• W2808068377 cites W4235557336 @default.
• W2808068377 cites W819456204 @default.
• W2808068377 doi "https://doi.org/10.1016/j.tplants.2018.05.011" @default.
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