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2.  The iron deficiency-induced phenolics secretion plays multiple important roles in plant iron acquisition underground 
Plant Signaling & Behavior  2008;3(1):60-61.
In non-graminaceous monocots and dicots, phenolic compounds are frequently reported to be the main components of root exudates in response to Fe deficiency. We show that the phenolics secretion is an important part of a plant's adaptive strategy to Fe deficiency stress that encourages a reutilization of the considerable amounts of Fe normally stored and unavailable in the root apoplast. Besides, we also found that the secreted phenolics can selectively alter the soil microbial community, and the altered soil microbial community may in turn favor plant Fe acquisition by producing siderophores and auxins.
PMCID: PMC2633963  PMID: 19704773
iron deficiency; phenolics; reutilization; soil microorganism; siderophore; auxins
3.  The Iron-Deficiency Induced Phenolics Accumulation May Involve in Regulation of Fe(III) Chelate Reductase in Red Clover 
Plant Signaling & Behavior  2007;2(5):327-332.
Although considerable researches have been conducted on the physiological responses to plant iron (Fe) deficiency stress in dicotyledonous plants, much still needs to be learned about the regulation of these processes. In the present research, red clover was used to investigate the role of root phenolics accumulation in regulating Fe-deficiency induced Fe(III) chelate reductase (FCR). The root FCR activity, IAA and phenolics accumulation, and also the phenolics secretion were greatly increased by the Fe deficiency treatment. The application of TIBA (2,3,5-triiodobenoic acid) to the stem, an IAA polar transport inhibitor, which could decrease IAA accumulation in root, significantly inhibited the FCR activity, but did not effect root phenolics accumulation and secretion, suggesting that IAA itself did not involve in root phenolics accumulation and secretion. In contrast, the Fe deficiency treatment significantly decreased the root IAA-oxidase activity. Interestingly the phenolics extracted from roots inhibited IAA-oxidase activity in vitro, and this inhibition was greater with phenolics extracted from roots of Fe deficient plants than that from Fe sufficient plants, indicating that the Fe deficiency-induced IAA-oxidase inhibition probably caused by the phenolics accumulation in Fe deficient roots. Based on these observations, we propose a model where under Fe deficiency stress in dicots, an increase in root phenolics concentrations plays a role in regulating root IAA levels through an inhibition of root IAA oxidase activity. This response, leads to, or at least partially leads to an increase in root IAA levels, which in turn help induce increased root FCR activity.
PMCID: PMC2634204  PMID: 19516996
Fe deficiency; ferric chelate reductase; phenolics; Trifolium pretense
4.  An underground tale: contribution of microbial activity to plant iron acquisition via ecological processes 
Annals of Botany  2013;113(1):7-18.
Iron (Fe) deficiency in crops is a worldwide agricultural problem. Plants have evolved several strategies to enhance Fe acquisition, but increasing evidence has shown that the intrinsic plant-based strategies alone are insufficient to avoid Fe deficiency in Fe-limited soils. Soil micro-organisms also play a critical role in plant Fe acquisition; however, the mechanisms behind their promotion of Fe acquisition remain largely unknown.
This review focuses on the possible mechanisms underlying the promotion of plant Fe acquisition by soil micro-organisms.
Fe-deficiency-induced root exudates alter the microbial community in the rhizosphere by modifying the physicochemical properties of soil, and/or by their antimicrobial and/or growth-promoting effects. The altered microbial community may in turn benefit plant Fe acquisition via production of siderophores and protons, both of which improve Fe bioavailability in soil, and via hormone generation that triggers the enhancement of Fe uptake capacity in plants. In addition, symbiotic interactions between micro-organisms and host plants could also enhance plant Fe acquisition, possibly including: rhizobium nodulation enhancing plant Fe uptake capacity and mycorrhizal fungal infection enhancing root length and the nutrient acquisition area of the root system, as well as increasing the production of Fe3+ chelators and protons.
PMCID: PMC3864720  PMID: 24265348
Hormones; iron deficiency; microbial community structure; siderophore; symbiosis
5.  The role of VuMATE1 expression in aluminium-inducible citrate secretion in rice bean (Vigna umbellata) roots 
Journal of Experimental Botany  2013;64(7):1795-1804.
Aluminium (Al)-activated citrate secretion plays an important role in Al resistance in a number of plant species, such as rice bean (Vigna umbellata). This study further characterized the regulation of VuMATE1, an aluminium-activated citrate transporter. Al stress induced VuMATE1 expression, followed by the secretion of citrate. Citrate secretion was specific to Al stress, whereas VuMATE1 expression was not, which could be explained by a combined regulation of VuMATE1 expression and Al-specific activation of VuMATE1 protein. Pre-treatment with a protein translation inhibitor suppressed VuMATE1 expression, indicating that de novo biosynthesis of proteins is required for gene expression. Furthermore, post-treatment with a protein translation inhibitor inhibited citrate secretion, indicating that post-transcriptional regulation of VuMATE1 is critical for citrate secretion. Protein kinase and phosphatase inhibitor studies showed that reversible phosphorylation was important not only for transcriptional regulation of VuMATE1 expression but also for post-translational regulation of VuMATE1 protein activity. These results suggest that citrate secretion is dependent on both transcriptional and post-transcriptional regulation of VuMATE1. Additionally, VuMATE1 promoter–β-glucuronidase fusion lines revealed that VuMATE1 expression was restricted to the root apex and was entirely Al induced, indicating the presence of cis-acting elements regulating root tip-specific and Al-inducible gene expression, which will be an important resource for genetic improvement of plant Al resistance.
PMCID: PMC3638816  PMID: 23408830
aluminium toxicity; cis-acting element; promoter; reversible phosphorylation; signalling transduction; transcription factor.
6.  Nitric oxide is the shared signalling molecule in phosphorus- and iron-deficiency-induced formation of cluster roots in white lupin (Lupinus albus) 
Annals of Botany  2012;109(6):1055-1064.
Background and Aims
Formation of cluster roots is one of the most specific root adaptations to nutrient deficiency. In white lupin (Lupinus albus), cluster roots can be induced by phosphorus (P) or iron (Fe) deficiency. The aim of the present work was to investigate the potential shared signalling pathway in P- and Fe-deficiency-induced cluster root formation.
Measurements were made of the internal concentration of nutrients, levels of nitric oxide (NO), citrate exudation and expression of some specific genes under four P × Fe combinations, namely (1) 50 µm P and 10 µm Fe (+P + Fe); (2) 0 P and 10 µm Fe (–P + Fe); (3) 50 µm P and 0 Fe (+P–Fe); and (4) 0 P and 0 Fe (–P–Fe), and these were examined in relation to the formation of cluster roots.
Key Results
The deficiency of P, Fe or both increased the cluster root number and cluster zones. It also enhanced NO accumulation in pericycle cells and rootlet primordia at various stages of cluster root development. The formation of cluster roots and rootlet primordia, together with the expression of LaSCR1 and LaSCR2 which is crucial in cluster root formation, were induced by the exogenous NO donor S-nitrosoglutathione (GSNO) under the +P + Fe condition, but were inhibited by the NO-specific endogenous scavenger 2-(4-carboxyphenyl)-4, 4, 5, 5-tetramethylimidazoline-1-oxyl- 3-oxide (cPTIO) under –P + Fe, +P–Fe and –P–Fe conditions. However, cluster roots induced by an exogenous supply of the NO donor did not secrete citrate, unlike those formed under –P or –Fe conditions.
NO plays an important role in the shared signalling pathway of the P- and Fe-deficiency-induced formation of cluster roots in white lupin.
PMCID: PMC3336943  PMID: 22351487
Cluster roots; gene expression; iron deficiency; nitric oxide; phosphorus deficiency; Lupinus albus
7.  TcOPT3, a Member of Oligopeptide Transporters from the Hyperaccumulator Thlaspi caerulescens, Is a Novel Fe/Zn/Cd/Cu Transporter 
PLoS ONE  2012;7(6):e38535.
Thlaspi caerulescens is a natural selected heavy metal hyperaccumulator that can not only tolerate but also accumulate extremely high levels of heavy metals in the shoots. Thus, to identify the transportors involved in metal long-distance transportation is very important for understanding the mechanism of heavy metal accumulation in this hyperaccumulator.
Methodology/Principal Findings
We cloned and characterized a novel gene TcOPT3 of OPT family from T. caerulescens. TcOPT3 was pronouncedly expressed in aerial parts, including stem and leaf. Moreover, in situ hybridization analyses showed that TcOPT3 expressed in the plant vascular systems, especially in the pericycle cells that may be involved in the long-distance transportation. The expression of TcOPT3 was highly induced by iron (Fe) and zinc (Zn) deficiency, especially in the stem and leaf. Sub-cellular localization showed that TcOPT3 was a plasma membrane-localized protein. Furthermore, heterogonous expression of TcOPT3 by mutant yeast (Saccharomyces cerevisiae) complementation experiments demonstrated that TcOPT3 could transport Fe2+ and Zn2+. Moreover, expression of TcOPT3 in yeast increased metal (Fe, Zn, Cu and Cd) accumulation and resulted in an increased sensitivity to cadmium (Cd) and copper (Cu).
Our data demonstrated that TcOPT3 might encode an Fe/Zn/Cd/Cu influx transporter with broad-substrate. This is the first report showing that TcOPT3 may be involved in metal long-distance transportation and contribute to the heavy metal hyperaccumulation.
PMCID: PMC3382247  PMID: 22761683
8.  Genotypic differences in Al resistance and the role of cell-wall pectin in Al exclusion from the root apex in Fagopyrum tataricum 
Annals of Botany  2010;107(3):371-378.
Background and Aims
Aluminium (Al) toxicity is one of the factors limiting crop production on acid soils. However, genotypic differences exist among plant species or cultivars in response to Al toxicity. This study aims to investigate genotypic differences among eight cultivars of tatary buckwheat (Fagopyrum tataricum) for Al resistance and explore the possible mechanisms of Al resistance.
Al resistance was evaluated based on relative root elongation (root elongation with Al/root elongation without Al). Root apex Al content, pectin content and exudation of root organic acids were determined and compared.
Key Results
Genotypic differences among the eight cultivars were correlated with exclusion of Al from the root apex. However, there was a lack of correlation between Al exclusion and Al-induced oxalate secretion. Interestingly, cell-wall pectin content of the root apex was generally lower in Al-resistant cultivars than in Al-sensitive cultivars. Although we were unable to establish a significant correlation between Al exclusion and pectin content among the eight cultivars, a strong correlation could be established among six cultivars, in which the pectin content in the most Al-resistant cultivar ‘Chuan’ was significantly lower than that in the most Al-sensitive cultivar ‘Liuku2’. Furthermore, root apex cell-wall pectin methylesterase activity (PME) was similar in ‘Chuan’ and ‘Liuku2’ in the absence of Al, but Al treatment resulted in increased PME activity in ‘Liuku2’ compared with ‘Chuan’. Immunolocalization of pectins also showed that the two cultivars had similar amounts of either low-methyl-ester pectins or high-methyl-ester pectins in the absence of Al, but Al treatment resulted in a more significant increase of low-methyl-ester pectins and decrease of high-methyl-ester pectins in ‘Liuku2’.
Cell-wall pectin content may contribute, at least in part, to differential Al resistance among tatary buckwheat cultivars.
PMCID: PMC3043930  PMID: 21183454
Aluminium resistance; cell wall; exclusion mechanism; Fagopyrum tataricum; pectin; pectin methylesterase; oxalate; toxicity
9.  Crop production on acidic soils: overcoming aluminium toxicity and phosphorus deficiency 
Annals of Botany  2010;106(1):183-184.
PMCID: PMC2889811  PMID: 20570831
10.  Disorganized distribution of homogalacturonan epitopes in cell walls as one possible mechanism for aluminium-induced root growth inhibition in maize 
Annals of Botany  2009;104(2):235-241.
Background and Aims
Aluminium (Al) toxicity is one of the most severe limitations to crop production in acid soils. Inhibition of root elongation is the primary symptom of Al toxicity. However, the underlying basis of the process is unclear. Considering the multiple physiological and biochemical functions of pectin in plants, possible involvement of homogalacturonan (HG), one of the pectic polysaccharide domains, was examined in connection with root growth inhibition induced by Al.
An immunolabelling technique with antibodies specific to HG epitopes (JIM5, unesterified residues flanked by methylesterifed residues; JIM7, methyl-esterified residues flanked by unesterified residues) was used to visualize the distribution of different types of HG in cell walls of root apices of two maize cultivars differing in Al resistance.
Key Results
In the absence of Al, the JIM5 epitope was present around the cell wall with higher fluorescence intensity at cell corners lining the intercellular spaces, and the JIM7 epitope was present throughout the cell wall. However, treatment with 50 µm Al for 3 h produced 10 % root growth inhibition in both cultivars and caused the disappearance of fluorescence in the middle lamella of both epitopes. Prolonged Al treatment (24 h) with 50 % root growth inhibition in ‘B73’, an Al-sensitive cultivar, resulted in faint and irregular distribution of both epitopes. In ‘Nongda3138’, an Al-resistant cultivar, the distribution of HG epitopes was also restricted to the lining of intercellular spaces when a 50 % inhibition to root growth was induced by Al (100 µm Al, 9 h). Altered distribution of both epitopes was also observed when of roots were exposed to 50 µm LaCl3 for 24 h, resulting in 40 % inhibition of root growth.
Changes in HG distribution and root growth inhibition were highly correlated, indicating that Al-induced perturbed distribution of HG epitopes is possibly involved in Al-induced inhibition of root growth in maize.
PMCID: PMC2710910  PMID: 19483201
Al toxicity; cell wall; homogalacturnonan; immunofluorescence; methylesterification; pectin
11.  Citrate Transporters Play a Critical Role in Aluminium-stimulated Citrate Efflux in Rice Bean (Vigna umbellata) Roots 
Annals of Botany  2006;97(4):579-584.
• Background and Aims Aluminium (Al) stimulates the efflux of citrate from apices of rice bean (Vigna umbellata) roots. This response is delayed at least 3 h when roots are exposed to 50 µm Al, indicating that some inducible processes leading to citrate efflux are involved. The physiological bases responsible for the delayed response were examined here.
• Methods The effects of several antagonists of anion channels and citrate carriers, and of the protein synthesis inhibitor, cycloheximide (CHM) on Al-stimulated citrate efflux and/or citrate content were examined by high-pressure liquid chromatography (HPLC) or an enzymatic method.
• Key Results Both anion channel inhibitors and citrate carrier inhibitors can inhibit Al-stimulated citrate efflux, with anthracene-9-carboxylic acid (A-9-C, an anion channel inhibitor) and phenylisothiocyanate (PI, a citrate carrier inhibitor) the most effective inhibitors. A 6 h pulse of 50 µm Al induced a significant increase of citrate content in root apices and release of citrate. However, the increase in citrate content preceded the efflux. Furthermore, the release of citrate stimulated by the pulse treatment was inhibited by both A-9-C and PI, indicating the importance of the citrate carrier on the mitochondrial membrane and the anion channel on the plasma membrane for the Al-stimulated citrate efflux. CHM (20 µm) also significantly inhibited Al-stimulated citrate efflux, confirming that de novo protein synthesis is required for Al-stimulated citrate efflux.
• Conclusions These results indicate that the activation of genes possibly encoding citrate transporters plays a critical role in Al-stimulated citrate efflux.
PMCID: PMC2803670  PMID: 16446286
Aluminium resistance; anion channel; citrate carrier; inhibitor; organic acid anions; protein synthesis; rice bean; toxicity; transporter; Vigna umbellata

Results 1-11 (11)