Transcriptional profiling of aluminum toxicity and tolerance responses in maize roots
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ABSTRACT:
ORGANISM(S): Zea mays
PROVIDER: GSE10308 | GEO | 2008/01/29
SECONDARY ACCESSION(S): PRJNA108531
REPOSITORIES: GEO
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Project description:Aluminum (Al) toxicity, which is caused by the solubilization of Al3 in acid soils resulting in inhibition of root growth and nutrient/water acquisition, is a serious limitation to crop production, because up to one-half of the world?s potentially arable land is acidic. To date, however, no Al tolerance genes have yet been cloned. The physiological mechanisms of tolerance are somewhat better understood; the major documented mechanism involves the Al-activated release of Al-binding organic acids from the root tip, preventing uptake into the primary site of toxicity. In this study, a quantitative trait loci analysis of Al tolerance in Arabidopsis was conducted, which also correlated Al tolerance quantitative trait locus (QTL) with physiological mechanisms of tolerance. The analysis identified two major loci, which explain approximately 40% of the variance in Al tolerance observed among recombinant inbred lines derived from Landsberg erecta (sensitive) and Columbia (tolerant). We characterized the mechanism by which tolerance is achieved, and we found that the two QTL cosegregate with an Al-activated release of malate from Arabidopsis roots. Although only two of the QTL have been identified, malate release explains nearly all (95%) of the variation in Al tolerance in this population. Al tolerance in Landsberg erecta Columbia is more complex genetically than physiologically, in that a number of genes underlie a single physiological mechanism involving root malate release. These findings have set the stage for the subsequent cloning of the genes responsible for the Al tolerance QTL, and a genomics-based cloning strategy and initial progress on this are also discussed. A replicate experimental design type is where a series of replicates are performed to evaluate reproducibility or as a pilot study to determine the appropriate number of replicates for a subsequent experiments. Computed
2007-08-09 | E-GEOD-7582 | biostudies-arrayexpress
Project description:Aluminum (Al) toxicity, which is caused by the solubilization of Al3 in acid soils resulting in inhibition of root growth and nutrient/water acquisition, is a serious limitation to crop production, because up to one-half of the world?s potentially arable land is acidic. To date, however, no Al tolerance genes have yet been cloned. The physiological mechanisms of tolerance are somewhat better understood; the major documented mechanism involves the Al-activated release of Al-binding organic acids from the root tip, preventing uptake into the primary site of toxicity. In this study, a quantitative trait loci analysis of Al tolerance in Arabidopsis was conducted, which also correlated Al tolerance quantitative trait locus (QTL) with physiological mechanisms of tolerance. The analysis identified two major loci, which explain approximately 40% of the variance in Al tolerance observed among recombinant inbred lines derived from Landsberg erecta (sensitive) and Columbia (tolerant). We characterized the mechanism by which tolerance is achieved, and we found that the two QTL cosegregate with an Al-activated release of malate from Arabidopsis roots. Although only two of the QTL have been identified, malate release explains nearly all (95%) of the variation in Al tolerance in this population. Al tolerance in Landsberg erecta Columbia is more complex genetically than physiologically, in that a number of genes underlie a single physiological mechanism involving root malate release. These findings have set the stage for the subsequent cloning of the genes responsible for the Al tolerance QTL, and a genomics-based cloning strategy and initial progress on this are also discussed. A replicate experimental design type is where a series of replicates are performed to evaluate reproducibility or as a pilot study to determine the appropriate number of replicates for a subsequent experiments. Keywords: replicate_design
2007-08-09 | GSE7582 | GEO
Project description:Aluminum (Al) toxicity, which is caused by the solubilization of Al3 in acid soils resulting in inhibition of root growth and nutrient/water acquisition, is a serious limitation to crop production, because up to one-half of the world?s potentially arable land is acidic. To date, however, no Al tolerance genes have yet been cloned. The physiological mechanisms of tolerance are somewhat better understood; the major documented mechanism involves the Al-activated release of Al-binding organic acids from the root tip, preventing uptake into the primary site of toxicity. In this study, a quantitative trait loci analysis of Al tolerance in Arabidopsis was conducted, which also correlated Al tolerance quantitative trait locus (QTL) with physiological mechanisms of tolerance. The analysis identified two major loci, which explain approximately 40% of the variance in Al tolerance observed among recombinant inbred lines derived from Landsberg erecta (sensitive) and Columbia (tolerant). We characterized the mechanism by which tolerance is achieved, and we found that the two QTL cosegregate with an Al-activated release of malate from Arabidopsis roots. Although only two of the QTL have been identified, malate release explains nearly all (95%) of the variation in Al tolerance in this population. Al tolerance in Landsberg erecta Columbia is more complex genetically than physiologically, in that a number of genes underlie a single physiological mechanism involving root malate release. These findings have set the stage for the subsequent cloning of the genes responsible for the Al tolerance QTL, and a genomics-based cloning strategy and initial progress on this are also discussed.
2007-05-04 | E-SMDB-4017 | biostudies-arrayexpress
Project description:Aluminum (Al) toxicity is a major factor limiting crop yields on acid soils. In maize, Al tolerance is a complex phenomenon involving multiple genes and physiological mechanisms yet uncharacterized. To begin elucidating the molecular basis of maize Al toxicity and tolerance, we performed a detailed temporal analysis of root gene expression under Al stress using microarrays with an Al-tolerant and an Al-sensitive maize genotype. Seedlings of both genotypes were grown in hydroponics in a full nutrient solution containing 39uM of free Al3+ activity. Root samples were collected at 'time zero', and after 2, 6 and 24 hours of treatment. Time course experiment with 0h, 2h, 6h and 24 hours of Al treatment in two maize genotypes contrasting for Al tolerance. The experimental design used for the microarray study was of two interconnected loops, and utilized a total of 16 slide sets. Samples collected from each genotype at one time point were contrasted with the previous and subsequent time points in a loop (4 time points x 2 genotypes = 8 slide sets). Additionally, the loops were interconnected (with dye swap) so that the two genotypes were contrasted directly at each time point (4 time points x 2 replicates = 8 slide sets). The design was balanced for dye distribution throughout samples and biological replicates. Each sample was labeled twice with Cy3 and twice with Cy5; each biological replicate had four samples labeled with Cy3 and four samples labeled with Cy5. The Sample signal intensity values were log2 transformed and analyzed by two interconnected ANOVA mixed models using PROC MIXED in SAS (Jin et al., 2001; Wolfinger et al., 2001). The normalization ANOVA model yij = µ + Ai + Dj + (A x D)ij + eij was applied to account for experiment-wide sources of variation associated with array (Ai, degrees of freedom (df) = 15, random effect), dye (Dj, df = 1, fixed effect), and their interactions. The residuals (eij) were treated as normalized values and analyzed in the following ANOVA model (gene model), where effects were evaluated for each gene individually: rikl = µ + Ai + Gk + Tl + (G x T)kl + ekl. Gk is the kth genotype (i.e. C100-6 or L53; df = 1) and represents the effect of each genotype on the expression of every gene, Tl represents the lth treatment (i.e. 0, 2, 6 or 24 hours of Al treatment; df = 3), and (G x T)kl the interaction between genotype and treatment (df = 3). Array (Ai) was included as a random effect to control for spot effects (Jin et al., 2001). Least square means were calculated, and estimates of differential expression were calculated as the difference between least-square means for each of the terms in the model. ANOVA results linked below as Supplementary files.
2010-05-26 | E-GEOD-10308 | biostudies-arrayexpress
Project description:Gene expression profiling in soybean under aluminum stress: mechanisms of magnesium amelioration of aluminum toxicity at gene expression level. Micro-molar concentrations of magnesium in culture solution has been shown to ameliorate Al toxicity in soybean and other leguminous species. Different theories have been proposed to explain the chemical mechanisms of how the two ions interact to neutralize the toxic effect of aluminum in the plant root system. To understand the molecular mechanisms of the phenomenon at the gene expression level in soybean, we undertook a comparative transcriptome analysis in Al-tolerant and Al-sensitive genotypes treated with aluminum alone or aluminum plus magnesium using DNA microarrays. The results revealed magnesium enhances Al-tolerance level in the Al-tolerant genotype by down-regulating genes commonly induced in response to Al toxicity. We hypothesized that the magnesium-mediated alleviation of Al toxicity in the Al-tolerant genotype emanates from reduction in energy expenditure of gene expression induced in response to Al stress. Conversely, magnesium appears to ameliorate Al toxicity in the sensitive genotype by dual mechanisms of increasing the expression level of several genes involved in Al-tolerance and decreasing the expression level of most genes. Keywords: Soybean, aluminum toxicity, magnesium, transcriptome
2010-10-04 | GSE18518 | GEO
Project description:Gene expression profiling in soybean under aluminum stress: Transcriptome response to Al stress in roots of Al-tolerant genotype (PI 416937). Aluminum (Al) toxicity is a major constraint of crop production on acid soils. Many commercial soybean cultivars and advanced breeding lines have been evaluated for Al tolerance. Aluminum tolerance is quantitatively inherited trait in soybean making it difficult for genetic improvement. Understanding the molecular and genetic mechanisms of tolerance is crucial for developing efficient and effective programs aimed at improving Al tolerance trait The molecular mechanisms of Al tolerance is poorly understood in soybean. The objective of the research was to identify candidate aluminum tolerance genes in soybean Al-tolerant soybean genotype PI 416937 seedlings were exposed to zero or 10 µM Al in growth chamber under hydroponic conditions for four time span of 2, 12, 48 and 72 hrs in a randomized complete block design with three replications. Microarray analysis was made on mRNA isolated from 1 cm log tap root tips using Affymetrix soybean array with over 68,000 probe sets Glycine max L and wild soybean combined. Both novel and known genes were discovered in response to Al treatment. They include Al tolerance relevant proteins, families of transcription factors, zinc finger, bZIP, WRKY, MYB, ADR6, and NAC domain proteins were induced likely regulating Al tolerance downstream genes. Stress related proteins, cytochrome P450, glutathione-s transferase, glutaredoxin family and ascorbic acid biosynthesis protein were induced as signatures of cellular detoxification mechanisms. An ABC type multidrug resistance protein that could act as citrate transporter or Al exporter was up-regulated, a key Al tolerance mechanisms in several species. A cell wall loosening enzyme endoxylglucan hydrolases were also up-regulated probably reversing the wall rigidification caused by Al and promoting root growth under Al stress. Phytosulfokines growth factor involved in cell division and proliferation was up-regulated likely as a direct counter action to Al toxicity which inhibits root growth by limiting cell division and elongation. In conclusion, the Al tolerance candidate genes identified herein are potential targets for future genetic engineering and molecular breeding work on Al tolerance trait in soybean which in turn would contribute to gain in soybean productivity on acid soils.
2011-10-05 | GSE18423 | GEO
Project description:Gene expression profiling in soybean under aluminum stress: mechanisms of magnesium amelioration of aluminum toxicity at gene expression level. Micro-molar concentrations of magnesium in culture solution has been shown to ameliorate Al toxicity in soybean and other leguminous species. Different theories have been proposed to explain the chemical mechanisms of how the two ions interact to neutralize the toxic effect of aluminum in the plant root system. To understand the molecular mechanisms of the phenomenon at the gene expression level in soybean, we undertook a comparative transcriptome analysis in Al-tolerant and Al-sensitive genotypes treated with aluminum alone or aluminum plus magnesium using DNA microarrays. The results revealed magnesium enhances Al-tolerance level in the Al-tolerant genotype by down-regulating genes commonly induced in response to Al toxicity. We hypothesized that the magnesium-mediated alleviation of Al toxicity in the Al-tolerant genotype emanates from reduction in energy expenditure of gene expression induced in response to Al stress. Conversely, magnesium appears to ameliorate Al toxicity in the sensitive genotype by dual mechanisms of increasing the expression level of several genes involved in Al-tolerance and decreasing the expression level of most genes. Keywords: Soybean, aluminum toxicity, magnesium, transcriptome Two genotypes: PI 416937 (p) and Young (y); two treatments: Aluminum (Al) or Al+magnesium (Mg); two time points: 12 and 72 hrs; 3 replicates.
2010-10-04 | E-GEOD-18518 | biostudies-arrayexpress
Project description:Aluminum toxicity is one of the most important abiotic stresses that affects crop production worldwide. The soluble form (Al3+) inhibits root growth, altering water and nutrients uptake reducing the plant growth and development. Under a long term of Al3+ exposure, plants can activate several tolerance mechanisms and, to date, there are no reports of large-scale proteomic data of maize in response to this ion. To investigate the post-transcriptional regulation in response to Al toxicity, we performed a label-free quantitative proteomics for comparative analysis of two Al-contrasting popcorn inbred lines and an Al-tolerant commercial hybrid during 72 h under Al-stress. A total of 489 differentially accumulated proteins (DAPs) were identified in the Al-sensitive inbred line, 491 in the Al-tolerant inbred line, and 277 in the commercial hybrid. Among then, 120 DAPs were co-expressed in both Al tolerant genotypes. Bioinformatics analysis indicated that starch and sucrose metabolism, glycolysis/gluconeogenesis, and carbohydrate metabolism were significant biochemical process regulated in response to Al toxicity. The up-accumulation of sucrose synthase and the increased of sucrose content and starch degradation suggest that these components may be enhance popcorn tolerance to Al stress. The up-accumulation of citrate synthase suggests a key role of this enzyme in the detoxification process in the Al-tolerant inbred line. The integration of transcriptomic and proteomic data indicated that Al tolerance response presents a complex regulatory network into the transcription and translation dynamics of popcorn roots development.
2023-05-22 | PXD027588 | Pride
Project description:Gene expression profiling in soybean under aluminum stress: Transcriptome response to Al stress in roots of Al-tolerant genotype (PI 416937). Aluminum (Al) toxicity is a major constraint of crop production on acid soils. Many commercial soybean cultivars and advanced breeding lines have been evaluated for Al tolerance. Aluminum tolerance is quantitatively inherited trait in soybean making it difficult for genetic improvement. Understanding the molecular and genetic mechanisms of tolerance is crucial for developing efficient and effective programs aimed at improving Al tolerance trait The molecular mechanisms of Al tolerance is poorly understood in soybean. The objective of the research was to identify candidate aluminum tolerance genes in soybean Al-tolerant soybean genotype PI 416937 seedlings were exposed to zero or 10 µM Al in growth chamber under hydroponic conditions for four time span of 2, 12, 48 and 72 hrs in a randomized complete block design with three replications. Microarray analysis was made on mRNA isolated from 1 cm log tap root tips using Affymetrix soybean array with over 68,000 probe sets Glycine max L and wild soybean combined. Both novel and known genes were discovered in response to Al treatment. They include Al tolerance relevant proteins, families of transcription factors, zinc finger, bZIP, WRKY, MYB, ADR6, and NAC domain proteins were induced likely regulating Al tolerance downstream genes. Stress related proteins, cytochrome P450, glutathione-s transferase, glutaredoxin family and ascorbic acid biosynthesis protein were induced as signatures of cellular detoxification mechanisms. An ABC type multidrug resistance protein that could act as citrate transporter or Al exporter was up-regulated, a key Al tolerance mechanisms in several species. A cell wall loosening enzyme endoxylglucan hydrolases were also up-regulated probably reversing the wall rigidification caused by Al and promoting root growth under Al stress. Phytosulfokines growth factor involved in cell division and proliferation was up-regulated likely as a direct counter action to Al toxicity which inhibits root growth by limiting cell division and elongation. In conclusion, the Al tolerance candidate genes identified herein are potential targets for future genetic engineering and molecular breeding work on Al tolerance trait in soybean which in turn would contribute to gain in soybean productivity on acid soils. One genotype PI 416937 (p); four time points: (2, 12, 48, and 72 hrs), with replicates (2 or 3)
2011-10-04 | E-GEOD-18423 | biostudies-arrayexpress
Project description:Background Ionic aluminum (mainly Al3+) is rhizotoxic and can be present in acid soils at concentrations high enough to inhibit root growth. Many forest tree species grow naturally in acid soils and often tolerate high concentrations of Al. Previously, we have shown that aspen (Populus tremula) releases citrate and oxalate from roots in response to Al exposure. To obtain further insights into the root responses of aspen to Al, we investigated root gene expression at Al conditions that inhibit root growth. Results Treatment of the aspen roots with 500 µM Al induced a strong inhibition of root growth within 6 h of exposure time. The root growth subsequently recovered, reaching growth rates comparable to that of control plants. Changes in gene expression were determined after 6 h, 2 d, and 10 d of Al exposure. Replicated transcriptome analyses using the Affymetrix poplar genome array revealed a total of 175 significantly up-regulated and 69 down-regulated genes, of which 70% could be annotated based on Arabidopsis genome resources. Between 6 h and 2 d, the number of responsive genes strongly decreased from 202 to 26, and then the number of changes remained low. The responses after 6 h were characterized by genes involved in cell wall modification, ion transport, and oxidative stress. Two genes with prolonged induction were closely related to the Arabidopsis Al tolerance genes ALS3 (for Al sensitive 3) and MATE (for multidrug and toxin efflux protein, mediating citrate efflux). Patterns of expression in different plant organs and in response to Al indicated that the two aspen genes are homologs of the Arabidopsis ALS3 and MATE. Conclusion Exposure of aspen roots to Al results in a rapid inhibition of root growth and a large change in root gene expression. The subsequent root growth recovery and the concomitant reduction in the number of responsive genes presumably reflect the success of the roots in activating Al tolerance mechanisms. The aspen genes ALS3 and MATE may be important components of these mechanisms.
2010-08-24 | GSE19297 | GEO