Comparative Long Non-Coding Transcriptome Analysis of Three Contrasting Barley Varieties in Response to Aluminum Stress.

Aluminum toxicity is a major abiotic stress on acidic soils, leading to restricted root growth and reduced plant yield. Long non-coding RNAs are crucial signaling molecules regulating the expression of downstream genes, particularly under abiotic stress conditions. However, the extent to which lncRNAs participate in the response to aluminum (Al) stress in barley remains largely unknown. Here, we conducted RNA sequencing of root samples under aluminum stress and compared the lncRNA transcriptomes of two Tibetan wild barley genotypes, XZ16 (Al-tolerant) and XZ61 (Al-sensitive), as well as the aluminum-tolerant cultivar Dayton. In total, 268 lncRNAs were identified as aluminum-responsive genes on the basis of their differential expression profiles under aluminum treatment. Through target gene prediction analysis, we identified 938 candidate lncRNA-messenger RNA (mRNA) pairs that function in a cis-acting manner. Subsequently, enrichment analysis showed that the genes targeted by aluminum-responsive lncRNAs were involved in diterpenoid biosynthesis, peroxisome function, and starch/sucrose metabolism. Further analysis of genotype differences in the transcriptome led to the identification of 15 aluminum-responsive lncRNAs specifically altered by aluminum stress in XZ16. The RNA sequencing data were further validated by RT-qPCR. The functional roles of lncRNA-mRNA interactions demonstrated that these lncRNAs are involved in the signal transduction of secondary messengers, and a disease resistance protein, such as RPP13-like protein 4, is probably involved in aluminum tolerance in XZ16. The current findings significantly contribute to our understanding of the regulatory roles of lncRNAs in aluminum tolerance and extend our knowledge of their importance in plant responses to aluminum stress.

Commonalities and Specificities in Wheat (Triticum aestivum L.) Responses to Aluminum Toxicity and Low Phosphorus Revealed by Transcriptomics and Targeted Metabolomics.

Aluminum (Al) toxicity and low phosphorus availability (LP) are the top two co-existing edaphic constraints limiting agriculture productivity in acid soils. Plants have evolved versatile mechanisms to cope with the two stresses alone or simultaneously. However, the specific and common molecular mechanisms, especially those involving flavonoids and carbohydrate metabolism, remain unclear. Laboratory studies were conducted on two wheat genotypes-Fielder (Al-tolerant and P-efficient) and Ardito (Al-sensitive and P-inefficient)-exposed to 50 µM Al and 2 µM Pi (LP) in hydroponic solutions. After 4 days of stress, wheat roots were analyzed using transcriptomics and targeted metabolomics techniques. In Fielder, a total of 2296 differentially expressed genes (DEGs) were identified under Al stress, with 1535 upregulated and 761 downregulated, and 3029 DEGs were identified under LP stress, with 1591 upregulated and 1438 downregulated. Similarly, 4404 DEGs were identified in Ardito under Al stress, with 3191 upregulated and 1213 downregulated, and 1430 DEGs were identified under LP stress, with 1176 upregulated and 254 downregulated. GO annotation analysis results showed that 4079 DEGs were annotated to the metabolic processes term. These DEGs were significantly enriched in the phenylpropanoid, flavonoid, flavone and flavonol biosynthesis, and carbohydrate metabolism pathways by performing the KEGG enrichment analysis. The targeted metabolome analysis detected 19 flavonoids and 15 carbohydrate components in Fielder and Ardito under Al and LP stresses. In Fielder, more responsive genes and metabolites were involved in flavonoid metabolism under LP than Al stress, whereas the opposite trend was observed in Ardito. In the carbohydrate metabolism pathway, the gene and metabolite expression levels were higher in Fielder than in Ardito. The combined transcriptome and metabolome analysis revealed differences in flavonoid- and carbohydrate-related genes and metabolites between Fielder and Ardito under Al and LP stresses, which may contribute to Fielder's higher resistance to Al and LP. The results of this study lay a foundation for pyramiding genes and breeding multi-resistant varieties.

Therapeutic effects of a new bithiophene against aluminum -induced Alzheimer's disease in a rat model: Pathological and ultrastructural approach.

Alzheimer's disease (AD) remains of unknown etiology and lacks a cure. This study aimed to evaluate the therapeutic potential of a novel bithiophene derivative at two doses against AlCl3-induced AD in a rat model. Adult male rats (Rattus norvegicus) were divided into six groups (n=6): Group one consisted of naïve animals, group two received bithiophene (1 mg/kg) every other day for 30 days, and groups 3-6 were subjected to AlCl3 (100 mg/kg, equivalent to 20.23 mg Al3+) for 45 consecutive days. Groups four and five received low (0.5 mg/kg) or high (1 mg/kg) doses of bithiophene, respectively. Group six received memantine (20 mg/kg) daily for 30 days. All treatments were administered orally. Aluminum exposure resulted in severe degeneration of both histological and ultrastructural aspects of cells. Administration of the low dose of bithiophene significantly restored the number of CA1 pyramidal cells and the thickness of the stratum granulosum of the dentate gyrus. However, the high dose of bithiophene increased viable CA1 pyramidal cell numbers significantly without restoring the thickness of the stratum granulosum or reducing vacuolization or pyknotic changes. The low dose of bithiophene restored the normal histological and cytological structure of both cortical and hippocampal neurons affected by dementia. Further investigation is required to explore the molecular mechanisms underlying the ameliorative effects on Alzheimer's disease-induced deteriorations in the cortex and hippocampus.

Long-term evaluation of potential Al toxicity after an Al treatment in a coastal bay.

Coastal areas often suffer from eutrophication, causing ecosystem degradation and oxygen deficiencies. In hundreds of lakes, aluminium (Al) treatment has been a successful method to bind phosphorous in the sediments, reducing lake productivity. In this study we follow up a successful Al treatment of the sediment of Björnöfjärden, which was the first full-scale coastal remediation project using a geo-engineering method, that substantially reduced P concentrations in the water column. We evaluate the long-term development of Al in the water and aquatic life using 10 years data from before, during and after the aluminium treatment. Still after ten years, the treatment is successful with low P concentrations in the Bay. After a temporal increase of Al in water and biota (fish and algae) in connection with the Al treatment, the concentration decreased rapidly to pre-treatment levels. A risk assessment for biota and humans consuming fish and water from the bay showed that the risk for negative effects were negligible, also during the treatment year.

Systematic Investigation of Aluminum Stress-Related Genes and Their Critical Roles in Plants.

Aluminum (Al) stress is a dominant obstacle for plant growth in acidic soil, which accounts for approximately 40-50% of the world's potential arable land. The identification and characterization of Al stress response (Al-SR) genes in Arabidopsis, rice, and other plants have deepened our understanding of Al's molecular mechanisms. However, as a crop sensitive to acidic soil, only eight Al-SR genes have been identified and functionally characterized in maize. In this review, we summarize the Al-SR genes in plants, including their classifications, subcellular localizations, expression organs, functions, and primarily molecular regulatory networks. Moreover, we predict 166 putative Al-SR genes in maize based on orthologue analyses, facilitating a comprehensive understanding of the impact of Al stress on maize growth and development. Finally, we highlight the potential applications of alleviating Al toxicity in crop production. This review deepens our understanding of the Al response in plants and provides a blueprint for alleviating Al toxicity in crop production.

A Brief Review of Effects of Aluminum on Marine Diatoms.

Aluminum (Al) is the most abundant metal element in the Earth's crust, yet it is present in trace levels in seawater. Growing evidence suggests potential effects of Al on the biogeochemical cycles of carbon (C) and silicon (Si) in the marine environment. By accumulation, sinking, and deposition, diatoms play a center role in coupling these three elements' biocycles in the oceans. However, it is still a challenge to elucidate the behaviors of diatoms influenced by Al. Our review aims to present the current knowledge of Al biogeochemistry in marine environment and its impact on marine phytoplankton, with a focus on how Al influences diatoms. Previous researches indicate that Al can promote the growth of diatoms, and diatoms have the ability to incorporate Al into their frustules. Given this, we paid particular attention on the interaction between Al and diatom frustules, and the influences of Al on the physiology and ecology of diatoms. Furthermore, it is suggested that Al alters the accumulation of other nutrients such as nitrogen, phosphorus and iron in diatoms; the subsequent responses of diatoms are also discussed. The objective of this review is to address the potential roles of Al in diatoms and offer insights into the possible biogeochemistry implications.

The White Matter Integrity and Functional Connection Differences of Fornix (Cres)/Stria Terminalis in Individuals with Mild Cognitive Impairment Induced by Occupational Aluminum Exposure.

Long-term aluminum (Al) exposure increases the risk of mild cognitive impairment (MCI). The aim of the present study was to investigate the neural mechanisms of Al-induced MCI. In our study, a total of 52 individuals with occupational Al exposure >10 years were enrolled and divided into two groups: MCI (Al-MCI) and healthy controls (Al-HC). Plasma Al concentrations and Montreal Cognitive Assessment (MoCA) score were collected for all participants. And diffusion tensor imaging and resting-state functional magnetic resonance imaging were used to examine changes of white matter (WM) and functional connectivity (FC). There was a negative correlation between MoCA score and plasma Al concentration. Compared with the Al-HC, fractional anisotropy value for the right fornix (cres)/stria terminalis (FX/ST) was higher in the Al-MCI. Furthermore, there was a difference in FC between participants with and without MCI under Al exposure. We defined the regions with differing FC as a "pathway," specifically the connectivity from the right temporal pole to the right FX/ST, then to the right sagittal stratum, and further to the right anterior cingulate and paracingulate gyri and right inferior frontal gyrus, orbital part. In summary, we believe that the observed differences in WM integrity and FC in the right FX/ST between participants with and without MCI under long-term Al exposure may represent the neural mechanisms underlying MCI induced by Al exposure.

Genomic selection for tolerance to aluminum toxicity in a synthetic population of upland rice.

Over half of the world's arable land is acidic, which constrains cereal production. In South America, different rice-growing regions (Cerrado in Brazil and Llanos in Colombia and Venezuela) are particularly affected due to high aluminum toxicity levels. For this reason, efforts have been made to breed for tolerance to aluminum toxicity using synthetic populations. The breeding program of CIAT-CIRAD is a good example of the use of recurrent selection to increase productivity for the Llanos in Colombia. In this study, we evaluated the performance of genomic prediction models to optimize the breeding scheme by hastening the development of an improved synthetic population and elite lines. We characterized 334 families at the S0:4 generation in two conditions. One condition was the control, managed with liming, while the other had high aluminum toxicity. Four traits were considered: days to flowering (FL), plant height (PH), grain yield (YLD), and zinc concentration in the polished grain (ZN). The population presented a high tolerance to aluminum toxicity, with more than 72% of the families showing a higher yield under aluminum conditions. The performance of the families under the aluminum toxicity condition was predicted using four different models: a single-environment model and three multi-environment models. The multi-environment models differed in the way they integrated genotype-by-environment interactions. The best predictive abilities were achieved using multi-environment models: 0.67 for FL, 0.60 for PH, 0.53 for YLD, and 0.65 for ZN. The gain of multi-environment over single-environment models ranged from 71% for YLD to 430% for FL. The selection of the best-performing families based on multi-trait indices, including the four traits mentioned above, facilitated the identification of suitable families for recombination. This information will be used to develop a new cycle of recurrent selection through genomic selection.

Both hormones and energy-rich compounds play a role in the mitigation of elevated pH on aluminum toxicity in Citrus sinensis leaves.

The contribution of plant hormones and energy-rich compounds and their metabolites (ECMs) in alleviating aluminum (Al) toxicity by elevated pH remains to be clarified. For the first time, a targeted metabolome was applied to identify Al-pH-interaction-responsive hormones and ECMs in Citrus sinensis leaves. More Al-toxicity-responsive hormones and ECMs were identified at pH 4.0 [4 (10) upregulated and 7 (17) downregulated hormones (ECMs)] than those at pH 3.0 [1 (9) upregulated and 4 (14) downregulated hormones (ECMs)], suggesting that the elevated pH improved the adaptation of hormones and ECMs to Al toxicity in leaves. The roles of hormones and ECMs in reducing leaf Al toxicity mediated by elevated pH might include the following aspects: (a) improved leaf growth by upregulating the levels of jasmonoyl-L-isoleucine (JA-ILE), 6-benzyladenosine (BAPR), N6-isopentenyladenosine (IPR), cis-zeatin-O-glucoside riboside (cZROG), and auxins (AUXs), preventing Al toxicity-induced reduction of gibberellin (GA) biosynthesis, and avoiding jasmonic acid (JA)-mediated defense; (b) enhanced biosynthesis and accumulation of tryptophan (TRP), as well as the resulting increase in biosynthesis of auxin, melatonin and secondary metabolites (SMs); (c) improved ability to maintain the homeostasis of ATP and other phosphorus (P)-containing ECMs; and (d) enhanced internal detoxification of Al due to increased organic acid (OA) and SM accumulation and elevated ability to detoxify reactive oxygen species (ROS) due to enhanced SM accumulation. To conclude, the current results corroborate the hypotheses that elevated pH reduces Al toxicity by upregulating the ability to maintain the homeostasis of ATP and other P-containing ECMs in leaves under Al toxicity and (b) hormones participate in the elevated pH-mediated alleviation of Al toxicity by positively regulating growth, the ability to detoxify ROS, and the internal detoxification of Al in leaves under Al toxicity. Our findings provide novel insights into the roles of hormones and ECMs in mitigating Al toxicity mediated by the elevated pH.

The tonoplast-localized OsTIP2;1 is involved in aluminum detoxification in rice.

Aluminum (Al) stress is a significant issue in acidic soils, severely affecting crop growth and yield. Rice is notably resilient to Al toxicity, yet the internal tolerance mechanisms remain inadequately addressed. Here, we examined the role of OsTIP2;1, a tonoplast-bound intrinsic protein (TIP), in rice's internal Al detoxification. Our findings reveal that OsTIP2;1 expression was quickly and explicitly activated by Al ions in roots but not in shoots. The OsTIP2;1-GFP protein localizes to the tonoplast in plant and yeast cells. Non-functional ostip2;1 rice mutants were more vulnerable to Al toxicity. In the roots, the ostip2;1 mutants exhibited considerably lower levels of Al in the cell sap, primarily the vacuolar contents, than in the wild-type plant. Moreover, the ostip2;1 mutants showed reduced Al accumulation in the roots but increased translocation to the shoots. Heterologous expression of tonoplast-localized OsTIP2;1 in yeast led to enhanced Al tolerance, suggesting that OsTIP2;1 facilitates Al sequestration to the vacuole. These findings indicate that OsTIP2;1 mediates internal detoxification by transporting Al into the vacuole in the root and restricting its transport to above-ground tissues, thus contributing to Al resistance in rice.

Aluminum causes irreversible damage to the development of hippocampal neurons by regulating m6A RNA methylation.

The underlying mechanism of the aluminum (Al) on neurotoxicity remains unclear. We explored whether the impairment of hippocampal neurons induced by developmental Al exposure was associated with the m6A RNA modification in mice. In this study, the pregnant female mice were administered 4 mg/mL aluminum-lactate from gestational day (GD) 6 to postnatal day (PND) 21. On PND 21, 10 offsprings per group were euthanized by exsanguination from the abdominal aorta after deep anesthetization. The other offsprings which treated with aluminum-lactate on maternal generation were divided into two groups and given 0 (PND60a) and 4 mg/mL (PND60b) aluminum-lactate in their drinking water until PND 60. Significant neuronal injuries of hippocampus as well as a reduction in the m6A RNA modification and the expression of methylase were observed at PND 21 and PND 60a mice. The results indicated that Al-induced developmental neurotoxicity could persist into adulthood despite no sustained Al accumulation. m6A RNA modification had a crucial role in developmental neurotoxicity induced by Al. In addition, Al exposure during the embryonic to adult stages can cause more severe nerve damage and decline of m6A RNA modification. Collectively, these results suggest that the mechanism underlying Al-induced neurotoxicity appears to involve m6A RNA modification.

Prenatal exposure to metal mixtures, body mass index trajectories in early life and effect modifiers: Insights from a prospective birth cohort study.

Current scientific knowledge is insufficient on the effects of metal mixtures on early life growth trajectories. This study included 7118 mother-infant pairs from a Chinese birth cohort. Concentrations of 18 maternal urinary metals were quantified, and growth trajectories were conducted based on standardized body mass index (BMI) for up to eight times from 0 to 2 years. A three-phase analytical framework was applied to explore the risk ratios (RR) and 95 % confidence intervals (95 % CI) of co-exposure to metals on dynamic growth, along with potential modifiers. Five growth trajectory groups were identified. Exposure to metal mixtures driven by thallium (Tl, 34.8 %) and aluminum (Al, 16.2 %) was associated with an increased risk of low-rising trajectory (RR=1.58, 95 % CI: 1.25, 2.00); however, exposure to mixtures driven by strontium (Sr, 49.5 %) exhibited an inverse correlation (RR = 0.81, 95 % CI: 0.67, 0.97). Furthermore, infants with varying levels of Tl, Al and Sr, as well as modifiers including pre-pregnancy BMI and infant sex faced distinct risks of low-rising trajectory. Our findings highlighted the Tl, Al, and Sr as key metals in relation to the low-rising trajectory in early life characterized as catch-up growth, with pre-pregnancy BMI and infant sex exerting as potential modifiers.

The RAE1-STOP1-GL2-RHD6 module regulates the ALMT1-dependent aluminum resistance in Arabidopsis.

Aluminum (Al) toxicity is one of the major constraints for crop production in acid soils, Al-ACTIVATED MALATE TRANSPORTER1 (ALMT1)-dependent malate exudation from roots is essential for Al resistance in Arabidopsis, in which the C2H2-type transcription factor SENSITIVE TO PROTONRHIZOTOXICITY1 (STOP1) play a critical role. In this study, we reveal that the RAE1-GL2-STOP1-RHD6 protein module regulated the ALMT1-mediated Al resistance. GL2, STOP1 and RHD6 directly target the promoter of ALMT1 to suppress or activate its transcriptional expression, respectively, and mutually influence their action on the promoter of ALMT1 by forming a protein complex. STOP1 mediates the expression of RHD6 and RHD6-regulated root growth inhibition, while GL2 and STOP1 suppress each other's expression at the transcriptional and translational level and regulate Al-inhibited root growth. F-box protein RAE1 degrades RHD6 via the 26S proteasome, leading to suppressed activity of the ALMT1 promoter. RHD6 inhibits the transcriptional expression of RAE1 by directly targeting its promoter. Unlike RHD6, RAE1 promotes the GL2 expression at the protein level and GL2 activates the expression of RAE1 at the transcriptional level by directly targeting its promoter. The study provides insights into the transcriptional regulation of ALMT1, revealing its significance in Al resistance and highlighting the crucial role of the STOP1-associated regulatory networks.

Naringenin mitigates nanoparticulate-aluminium induced neuronal degeneration in brain cortex and hippocampus through downregulation of oxidative stress and neuroinflammation.

Alumunium usage and toxicity has been a global concern especially an increased use of nanoparticulated aluminum (Al-NPs) products from the environment and the workplace. Al degrades in to nanoparticulate form in the environment due to the routine process of bioremediation in human body. Al-NPs toxicity plays key role in the pathophysiology of neurodegeneration which is characterised by the development of neurofibrillary tangles and neuritic plaques which correlates to the Alzheimer's disease. This study evaluated the Al-NPs induced neurodegeneration and causative behavioral alterations due to oxidative stress, inflammation, DNA damage, ß-amyloid aggregation, and histopathological changes in mice. Furthermore, the preventive effect of naringenin (NAR) as a potent neuroprotective flavonoid against Al-NPs induced neurodegeneration was assessed. Al-NPs were synthesized and examined using FTIR, XRD, TEM, and particle size analyzer. Mice were orally administered with Al-NPs (6 mg/kg b.w.) followed by NAR treatment (10 mg/kg b.w. per day) for 66 days. The spatial working memory was determined by novel object recognition, T-maze, Y-maze, and Morris Water Maze tests. We measured nitric oxide, advanced oxidation of protein products, protein carbonylation, lipid peroxidation, superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, reduced glutathione, oxidised glutathione, and acetylcholine esterase, as well as cytokines analysis, immunohistochemistry, and DNA damage. Al-NPs significantly reduced the learning memory power, increased oxidative stress, reduced antioxidant enzymatic activity, increased DNA damage, altered the levels of cytokines, and increased ß-amyloid aggregation in the cortex and hippocampus regions of the mice brain. These neurobehavioral impairments, neuronal oxidative stress, and histopathological alterations were significantly attenuated by NAR supplementation. In conclusion, Al-NPs may be potent neurotoxic upon exposure and that NAR could serve as a potential preventive measure in the treatment and management of neuronal degeneration.

Effects of copper, and aluminium in ionic, and nanoparticulate form on growth rate and gene expression of Setaria italica seedlings.

This study aims to determine the effects of copper, copper oxide nanoparticles, aluminium, and aluminium oxide nanoparticles on the growth rate and expression of ACT-1, CDPK, LIP, NFC, P5CR, P5CS, GR, and SiZIP1 genes in five days old seedling of Setaria italica ssp. maxima, cultivated in hydroponic culture. Depending on their concentration (ranging from 0.1 to 1.8 mg L-1), all tested substances had both stimulating and inhibiting effects on the growth rate of the seedlings. Copper and copper oxide-NPs had generally a stimulating effect whereas aluminium and aluminium oxide-NPs at first had a positive effect but in higher concentrations they inhibited the growth. Treating the seedlings with 0.4 mg L-1 of each tested toxicant was mostly stimulating to the expression of the genes and reduced the differences between the transcript levels of the coleoptiles and roots. Increasing concentrations of the tested substances had both stimulating and inhibiting effects on the expression levels of the genes. The highest expression levels were usually noted at concentrations between 0.4 and 1.0 mg/L of each metal and metal nanoparticle, except for SiZIP1, which had the highest transcript amount at 1.6 mg L-1 of Cu2+ and at 0.1-0.8 mg L-1 of CuO-NPs, and LIP and GR from the seedling treated with Al2O3-NPs at concentrations of 0.1 and 1.6 mg L-1, respectively.

Toxicity and biokinetics following pulmonary exposure to aluminium (aluminum): A review.

During the manufacture and use of aluminium (aluminum), inhalation exposure may occur. We reviewed the pulmonary toxicity of this metal including its toxicokinetics. The normal serum/plasma level based on 17 studies was 5.7 ± 7.7 µg Al/L (mean ± SD). The normal urine level based on 15 studies was 7.7 ± 5.3 µg/L. Bodily fluid and tissue levels during occupational exposure are also provided, and the urine level was increased in aluminium welders (43 ± 33 µg/L) based on 7 studies. Some studies demonstrated that aluminium from occupational exposure can remain in the body for years. Excretion pathways include urine and faeces. Toxicity studies were mostly on aluminium flakes, aluminium oxide and aluminium chlorohydrate as well as on mixed exposure, e.g. in aluminium smelters. Endpoints affected by pulmonary aluminium exposure include body weight, lung function, lung fibrosis, pulmonary inflammation and neurotoxicity. In men exposed to aluminium oxide particles (3.2 µm) for two hours, lowest observed adverse effect concentration (LOAEC) was 4 mg Al2O3/m3 (= 2.1 mg Al/m3), based on increased neutrophils in sputum. With the note that a similar but not statistically significant increase was seen during control exposure. In animal studies LOAECs start at 0.3 mg Al/m3. In intratracheal instillation studies, all done with aluminium oxide and mainly nanomaterials, lowest observed adverse effect levels (LOAELs) started at 1.3 mg Al/kg body weight (bw) (except one study with a LOAEL of ∼0.1 mg Al/kg bw). The collected data provide information regarding hazard identification and characterisation of pulmonary exposure to aluminium.

GmMYB183, a R2R3-MYB Transcription Factor in Tamba Black Soybean (Glycine max. cv. Tamba), Conferred Aluminum Tolerance in Arabidopsis and Soybean.

Aluminum (Al) toxicity is one of the environmental stress factors that affects crop growth, development, and productivity. MYB transcription factors play crucial roles in responding to biotic or abiotic stresses. However, the roles of MYB transcription factors in Al tolerance have not been clearly elucidated. Here, we found that GmMYB183, a gene encoding a R2R3 MYB transcription factor, is involved in Al tolerance. Subcellular localization studies revealed that GmMYB183 protein is located in the nucleus, cytoplasm and cell membrane. Overexpression of GmMYB183 in Arabidopsis and soybean hairy roots enhanced plant tolerance towards Al stress compared to the wild type, with higher citrate secretion and less Al accumulation. Furthermore, we showed that GmMYB183 binds the GmMATE75 gene promoter encoding for a plasma-membrane-localized citrate transporter. Through a dual-luciferase reporter system and yeast one hybrid, the GmMYB183 protein was shown to directly activate the transcription of GmMATE75. Furthermore, the expression of GmMATE75 may depend on phosphorylation of Ser36 residues in GmMYB183 and two MYB sites in P3 segment of the GmMATE75 promoter. In conclusion, GmMYB183 conferred Al tolerance by promoting the secretion of citrate, which provides a scientific basis for further elucidating the mechanism of plant Al resistance.

OsAlR3 regulates aluminum tolerance through promoting the secretion of organic acids and the expression of antioxidant genes in rice.

In acidic soils, aluminum (Al) toxicity inhibits the growth and development of plant roots and affects nutrient and water absorption, leading to reduced yield and quality. Therefore, it is crucial to investigate and identify candidate genes for Al tolerance and elucidate their physiological and molecular mechanisms under Al stress. In this study, we identified a new gene OsAlR3 regulating Al tolerance, and analyzed its mechanism from physiological, transcriptional and metabolic levels. Compared with the WT, malondialdehyde (MDA) and hydrogen peroxide (H2O2) content were significantly increased, superoxide dismutase (SOD) activity and citric acid (CA) content were significantly decreased in the osalr3 mutant lines when exposed to Al stress. Under Al stress, the osalr3 exhibited decreased expression of antioxidant-related genes and lower organic acid content compared with WT. Integrated transcriptome and metabolome analysis showed the phenylpropanoid biosynthetic pathway plays an important role in OsAlR3-mediated Al tolerance. Exogenous CA and oxalic acid (OA) could increase total root length and enhance the antioxidant capacity in the mutant lines under Al stress. Conclusively, we found a new gene OsAlR3 that positively regulates Al tolerance by promoting the chelation of Al ions through the secretion of organic acids, and increasing the expression of antioxidant genes.

Comparative transcriptome analyses reveal regulatory network and hub genes of aluminum response in roots of elephant grass (Cenchrus purpureus).

Aluminum (Al) toxicity severely restricts the growth and productivity of elephant grass in acidic soils around the world. However, the molecular mechanisms of Al response have not been investigated in elephant grass. In this study, we conducted phenotype, physiology, and transcriptome analysis of elephant grass roots in response to Al stress. Phenotypic analysis revealed that a low concentration of Al stress improved root growth while higher Al concentrations inhibit root growth. Al stress significantly increased the citrate (CA) content in roots, while the expression levels of genes related to citrate synthesis were substantially changed. The multidrug and toxic compound extrusion (MATE) family were identified as hub genes in the co-expression network of Al response in elephant grass roots. Phylogenetic analysis showed that hub genes CpMATE93 and CpMATE158 belonged to the same clade as other MATE genes reported to be involved in citrate transport. Additionally, overexpression of CpMATE93 conferred Al resistance in yeast cells. These results provide a theoretical basis for further studies of molecular mechanisms in the elephant grass response to Al stress and could help breeders develop elite cultivars with Al tolerance.