Mn Toxicity Research Articles

Hyperaccumulation of metal in the apoplast contributes to the tolerance of the phytoremediator Pistia stratiotes L. to manganese-contaminated water

Phytoremediation of manganese (Mn)-contaminated water requires the selection of Mn-tolerant species. This study reports on physiological changes and Mn bioaccumulation in the aquatic macrophyte Pistia stratiotes cultivated under various MnCl2 concentrations: control, 80, 340, 600, 1000, 2000, and 4000 µM. Few visual symptoms of Mn toxicity, such as chlorosis, were observed after 10 days, especially in plants treated with 2000 and 4000 µM MnCl2. High Mn accumulation was recorded, with maximum values of 23,700 and 24,600 µg g−1 DW in the shoots and roots, respectively, at 4000 µM Mn, contrasting with 825.01 and 1587.53 µg g−1 DW in control plants. Cellular fractioning showed that Mn in shoots and roots was mainly associated with the cell wall, with approximately 90% of the Mn in roots detected in the apoplast. There were no significant changes in net CO2 assimilation or respiratory rates after 5 and 10 days of Mn exposure. These results demonstrate that P. stratiotes is a Mn hyperaccumulator species with excellent phytoremediation potential, as shown by its high bioaccumulation capacity and its ability to maintain photosynthetic efficiency under Mn stress.

GmSTOP1-3 Increases Soybean Manganese Accumulation Under Phosphorus Deficiency by Regulating GmMATE2/13 and GmZIP6/GmIREG3.

Mineral nutrient deficiencies and metal ion toxicities coexist on acid soils. Phosphorus (P) deficiency in plants is generally accompanied with significant levels of leaf manganese (Mn) accumulation. However, the molecular regulatory mechanisms underpinning remain unclear. The present study found that P-deficient soybean plants accumulated more Mn compared to P-sufficient ones on acid soils in both field and greenhouse experiments. Meanwhile, both P deficiency and Mn toxicity enhanced the expression of GmSTOP1-3. Over-expressing GmSTOP1-3 enhanced Mn accumulation in transgenic soybean hairy roots, but RNA-interference did not show obvious differences. Moreover, transgenic soybeans with GmSTOP1-3-overexpression showed enhanced root citrate exudation and augmented Mn accumulation. RNA-sequence identified four downstream genes of GmSTOP1-3, including multidrug and toxic compound extrusion (GmMATE2/13) and metal transporter genes (GmZIP6/GmIREG3), which encode plasma membrane proteins. GmSTOP1-3 activated the transcription of these four genes by directly binding to their promoter regions. In addition, both GmZIP6 and GmIREG3 functioned in Mn uptake as manifested by the higher Mn concentration and decreased growth of soybean hairy roots with their overexpression. Taken together, it is suggested that upregulation of GmSTOP1-3 by low P stress on acid soils activates transcripts of GmMATE2/13 and GmZIP6/GmIREG3, which consequently result in enhanced Mn accumulation in soybean.

Study of excess manganese stress response highlights the central role of manganese exporter Mnx for holding manganese homeostasis in the cyanobacterium Synechocystis sp. PCC 6803.

Cellular levels of the essential micronutrient manganese (Mn) need to be carefully balanced within narrow borders. In cyanobacteria, a sufficient Mn supply is critical for ensuring the function of the oxygen-evolving complex as the central part of the photosynthetic machinery. However, Mn accumulation is fatal for the cells. The reason for the observed cytotoxicity is unclear. To understand the causality behind Mn toxicity in cyanobacteria, we investigated the impact of excess Mn on physiology and global gene expression in the model organism Synechocystis sp. PCC 6803. We compared the response of the WT and the knock-out mutant in the Mn exporter (Mnx), ∆mnx, which is disabled in the export of surplus Mn and thus functions as a model for toxic Mn overaccumulation. While growth and pigment accumulation in ∆mnx were severely impaired 24 h after the addition of tenfold Mn, the WT was not affected and thus mounted an adequate transcriptional response. RNA-seq data analysis revealed that the Mn stress transcriptomes partly resembled an iron limitation transcriptome. However, the expression of iron limitation signature genes isiABDC was not affected by the Mn treatment, indicating that Mn excess is not accompanied by iron limitation in Synechocystis. We suggest that the ferric uptake regulator, Fur, gets partially mismetallated under Mn excess conditions and thus interferes with an iron-dependent transcriptional response. To encounter mismetallation and other Mn-dependent problems on a protein level, the cells invest in transcripts of ribosomes, proteases and chaperones. In the case of the ∆mnx mutant, the consequences of the disability to export excess Mn from the cytosol manifest in additionally impaired energy metabolism and oxidative stress transcriptomes with a fatal outcome. This study emphasizes the central importance of Mn homeostasis and the transporter Mnx's role in restoring and holding it.

Plant Rho GTPase ROP6 Is Essential for Manganese Homeostasis in Arabidopsis.

Manganese (Mn) is an indispensable mineral for plant growth and development. However, plants cultivated in acidic and poorly drained soils are vulnerable to Mn2+ toxicity due to its heightened increased bioavailability. Despite the crucial roles of the Rho of plant (ROP) GTPases in various cellular processes, their precise function in regulating Mn homeostasis remains elusive. In this study, we unveil a novel ROP6 GTPase signalling pathway that profoundly influences Mn phytotoxicity tolerance in Arabidopsis. Remarkably, the rop6 and dominant-negative ROP6 (rop6DN) mutant plants displayed a dramatically sensitive phenotype to Mn toxicity, whereas ROP6-overexpression and constitutively activated ROP6 (rop6CA) lines exhibited enhanced Mn stress tolerance. Immunoblot analysis corroborated that the ROP6 protein, especially the active form of ROP6, increased in abundance in the presence of high Mn levels. Further, we identified that ROP6 physically interacted and colocalized with Metal Tolerance Protein 8 (MTP8) in vivo. Mn transport complementation assays in yeast, combined with biochemical analyses, emphasized the essentiality of ROP6 for MTP8's transport activity. In addition, genetic analyses indicated that ROP6 acted upstream of MTP8 in the regulatory cascade. Collectively, our findings elucidate that ROP6 GTPase signalling positively modulates and enhances Mn stress tolerance in plants.

An Overview of the Soil Acidity Causes in Ethiopia, Consequences, and Mitigation Strategies

Soil acidity is a serious land degradation problem and worldwide danger, impacting approximately 50% of the world's arable soils and limiting agricultural yield. Soil acidification is a complicated series of events that lead to the production of acidic soil. In its widest sense, it can be defined as the total of natural and human processes that reduce the pH of soil solutions. Soil acidity affects around 43% of agricultural land in Ethiopia's humid and sub humid highlands. The main objective of this seminar is to highlight different literatures on the concepts of soil acidity and to give a wealth of knowledge on the causes of soil acidity, the effects it has on agricultural production, and management strategies for reducing soil acidity and raising crop yield. Acid soils in western Ethiopia are mostly caused by topsoil erosion caused by heavy rains and high temperatures. This results in the loss of organic matter and the leaching of exchangeable basic cations (Ca<sup>2+</sup>, Mg<sup>2+</sup>, Na<sup>+</sup>, and K<sup>+</sup>). Because ammonium-based fertilizers are easily converted to nitrate and hydrogen ions in the soil, they play a significant role in acidification. One of the reasons of soil acidity is inefficient nitrogen usage, which is followed by alkalinity exports in crops. Soil acidity in Ethiopian highlands is mostly caused by the clearance of crop residues, continuous crop harvest without sufficient fertilization, cation removal, and usage of acid-forming inorganic fertilizers. Acid soil reduces nutrient availability and produces Al and Mn toxicity. In addition to these effects, soil acidity may rapidly degrade soil physicochemical qualities such as organic carbon (OC), cation exchange capacity (CEC), soil structure, porosity, and texture. Liming, the use of organic materials as ISFM, and the adoption of crop types that are resistant to Al toxicity are all alternatives for correcting acid soils. Liming can minimize toxicity by lowering concentrations, improving the availability of plant nutrients like P, Ca, Mg, and K in the soil, and reducing heavy metal solubility and leaching. Application of organic matter has a liming impact because of its abundance in alkaline cations (such Ca, Mg, and K) that were released from OM during mineralization. The pH of the soil is raised by soil organic matter, which helps with soil acidity supplements.

Dopaminergic REST/NRSF is protective against manganese-induced neurotoxicity in mice

Chronic exposure to elevated levels of manganese (Mn) may cause a neurological disorder referred to as manganism. The transcription factor REST is dysregulated in several neurodegenerative diseases, such as Alzheimer’s disease and Parkinson’s disease. REST upregulated tyrosine hydroxylase and induced protection against Mn toxicity in neuronal cultures. In the present study, we investigated if dopaminergic REST plays a critical role in protecting against Mn-induced toxicity in vivo using dopaminergic REST conditional knockout (REST-cKO) mice and REST loxP mice as wild-type (WT) controls. Restoration of REST in the substantia nigra (SN) with neuronal REST AAV vector infusion was performed to further support the role of REST in Mn toxicity. Mice were exposed to Mn (330 ug, intranasal, daily for 3 weeks), followed by behavioral tests and molecular biology experiments. Results showed that Mn decreased REST mRNA/protein levels in the SN-containing midbrain, as well as locomotor activity and motor coordination in WT mice, which were further decreased in REST-cKO. Mn-induced mitochondrial insults, such as impairment of fission/fusion and mitophagy, apoptosis, and oxidative stress, in the midbrain of WT mice were more pronounced in REST-cKO. However, REST restoration in the SN of REST cKO mice attenuated Mn-induced neurotoxicity. REST’s molecular target for its protection is unclear, but REST attenuated Mn-induced mitochondrial dysregulation, indicating that it is a primary intracellular target for both Mn and REST. These novel findings suggest that dopaminergic REST in the nigrostriatal pathway is critical in protecting against Mn toxicity, underscoring REST as a potential therapeutic target for treating manganism.

Phosphorus-induced restructuring of the ascorbate-glutathione cycle and lignin biosynthesis alleviates manganese toxicity in peach roots.

Manganese (Mn) is indispensable for plant growth, but its excessive uptake in acidic soils leads to toxicity, hampering food safety. Phosphorus (P) application is known to mitigate Mn toxicity, yet the underlying molecular mechanism remains elusive. Here, we conducted physiological and transcriptomic analyses of peach roots response to P supply under Mn toxicity. Manganese treatment disrupted root architecture and caused ultrastructural damage due to oxidative injury. Notably, P application ameliorated the detrimental effects and improved the damaged roots by preventing the shrinkage of cortical cells, epidermis and endodermis, as well as reducing the accumulation of reactive oxygen species (ROS). Transcriptomic analysis revealed the differentially expressed genes enriched in phenylpropanoid biosynthesis, cysteine, methionine and glutathione metabolism under Mn and P treatments. Phosphorus application upregulated the transcripts and activities of core enzymes crucial for lignin biosynthesis, enhancing cell wall integrity. Furthermore, P treatment activated ascorbate-glutathione cycle, augmenting ROS detoxification. Additionally, under Mn toxicity, P application downregulated Mn uptake transporter while enhancing vacuolar sequestration transporter transcripts, reducing Mn uptake and facilitating vacuolar storage. Collectively, P application prevents Mn accumulation in roots by modulating Mn transporters, bolstering lignin biosynthesis and attenuating oxidative stress, thereby improving root growth under Mn toxicity. Our findings provide novel insights into the mechanism of P-mediated alleviation of Mn stress and strategies for managing metal toxicity in peach orchards.

GmIRT1.1 from soybean (Glycine max L.) is involved in transporting Fe, Mn and Cd

Soybean is one of the most important crops for producing high quality oil and protein. Mineral nutrient deficiencies are frequently observed in soybeans. However, there are few studies to understand the absorption process of mineral nutrients in soybeans. Here, we investigated the functions of soybean (Glycine max L.) IRT1.1 (IRON-REGULATED TRANSPORTER 1.1) in the transportation of mineral elements. Heterologous expression of GmIRT1.1 in yeast mutants revealed that GmIRT1.1 compensated for the growth defects of Δfet3fet4 and Δsmf1 mutants under iron (Fe) and manganese (Mn) deficiency conditions, respectively, and enhanced the sensitivity of the Δycf1 mutant to cadmium (Cd) toxicity. Expression analysis revealed that GmIRT1.1 was only significantly induced by Fe deficiency and was primarily expressed in roots. Furthermore, the GmIRT1.1 overexpression lines enhanced Arabidopsis tolerance to Fe deficiency, leading to increased accumulation of Fe in the roots and shoots. Additionally, the transgenic lines increased the sensitivity to Mn and Cd toxicity. Subcellular localization analysis revealed that GmIRT1.1 was localized on the plasma membrane. Moreover, the results obtained from the soybean hairy roots system indicated that the localization of GmIRT1.1 was dependent on the regulation of Fe homeostasis in plant. Consequently, these results suggested that GmIRT1.1 was responsible for the transportation of Fe, Mn and Cd.

Transcriptome-wide m6A methylation and metabolomic analysis reveal regulatory networks in rice roots under manganese stress

Rice (Oryza sativa) has a higher tolerance to manganese (Mn) stress than other cereals. However, the regulatory mechanisms governing Mn tolerance in rice remain poorly understood. In this work, seedlings of the rice cultivar Nipponbare were treated with 1.0 mM MnCl2 for 10 days before root samples were collected for transcriptome-wide N6-methyladenosine (m6A) methylation and metabolome profiling. In the presence of extra Mn, we identified 2050 significantly modified m6A peaks and 2549 differentially expressed genes (DEGs). These DEGs were linked to key signaling pathways such as MAPK signaling, calcium signaling, and peroxides. Among these, 282 DEGs showed differential m6A methylation peaks, including 29 transcription factors, indicating they might be key upstream regulators of the Mn toxicity response. Furthermore, metabolomic research indicated considerable metabolic alterations in rice roots under Mn stress, notably in purine metabolism, amino acid biosynthesis, and glycerophospholipid metabolic pathways. Almost half of the metabolites were lipids or lipid-like compounds, indicating a potential function in signal transduction and membrane biogenesis. The findings lead to a better understanding of regulatory networks in rice roots that aid in Mn stress tolerance.

Manganese toxicity elicits the degradation of auxin transport carriers to restrain arabidopsis root growth

Manganese (Mn) is an essential microelement for plant growth but can be toxic when in excessive. Mn toxicity-inhibited root growth possible involves in auxin biosynthesis and transport in plants, but the mechanism remains elusive. Our results have suggested that Mn-inhibited root growth was possible associated with a reduced auxin levels in roots, as shown in experiments with (1) transgenic DII-VENUS and DR5rev::GFP; (2) the application of L-kynurenine (an inhibitor of TAA1 activity), 1-naphthylacetic acid (NAA), 1-naphthylphthalamic acid (NPA) to manipulate auxin levels; (3) using taa1 (defection in auxin biosynthesis) mutants; and (4) determining IAA by enzyme-linked immunosorbent assay. Those results were explained via down-regulated transcriptional levels of auxin biosynthesis-related genes in plants, and reduced abundance of PM-localized auxin transport carriers in roots. Combination of auxin transport-related transgenic pPINs-GFP or pAUX1::AUX1-YFP lines and a real-time in vitro observation of PM-localized PIN2/3/4 carriers using transgenic Dendra2 lines have revealed that excessive Mn induced degradation of these proteins, which might involve in Mn toxicity-elicited up-regulation of partially ubiquitin-, clathrin-meidiated endocytosis (CME)-, and endosomal sorting complex required for transport (ESCRT)-related genes. Overall, our results suggest that Mn toxicity reduces auxin level in the root apex possible via down-regulation of auxin biosynthesis-related genes and post-translational stimulation of the degradation of auxin transport proteins, leading to root growth inhibition caused by Mn toxicity.

Soil Acidity Causes in Ethiopia, Consequences and Mitigation Strategies-A Review

Soil acidity is a serious land degradation problem and worldwide danger, impacting approximately 50% of the world's arable soils and limiting agricultural yield. Soil acidification is a complicated series of events that lead to the production of acidic soil. In its widest sense, it can be defined as the total of natural and human processes that reduce the pH of soil solutions. Soil acidity affects around 43% of agricultural land in Ethiopia's humid and sub humid highlands. Acid soils in western Ethiopia are mostly caused by topsoil erosion caused by heavy rains and high temperatures. This results in the loss of organic matter and the leaching of exchangeable basic cations (Ca2+, Mg2+, Na+, and K+). Because ammonium-based fertilizers are easily converted to nitrate and hydrogen ions in the soil, they play a significant role in acidification. One of the reasons of soil acidity is inefficient nitrogen usage, which is followed by alkalinity exports in crops. Soil acidity in Ethiopian highlands is mostly caused by the clearance of crop residues, continuous crop harvest without sufficient fertilization, cation removal, and usage of acid-forming inorganic fertilizers. Acid soil reduces nutrient availability and produces Al and Mn toxicity. In addition to these effects, soil acidity may rapidly degrade soil physicochemical qualities such as organic carbon (OC), cation exchange capacity (CEC), soil structure, porosity, and texture. Liming, the use of organic materials as ISFM, and the adoption of crop types that are resistant to Al toxicity are all alternatives for correcting acid soils. Liming can minimize toxicity by lowering concentrations, improving the availability of plant nutrients like P, Ca, Mg, and K in the soil, and reducing heavy metal solubility and leaching. Application of organic matter has a liming impact because of its abundance in alkaline cations (such Ca, Mg, and K) that were released from OM during mineralization. The pH of the soil is raised by soil organic matter, which helps with soil acidity supplements.

Elevated thyroid manganese reduces thyroid iodine to induce hypothyroidism in mice, but not rats, lacking SLC30A10 transporter.

Elevated manganese (Mn) accumulates in the brain and induces neurotoxicity. SLC30A10 is an Mn efflux transporter that controls body Mn levels. We previously reported that full-body Slc30a10 knockout mice (1) recapitulate the body Mn retention phenotype of humans with loss-of-function SLC30A10 mutations and (2) unexpectedly develop hypothyroidism induced by Mn accumulation in the thyroid, which reduces intra-thyroid thyroxine. Subsequent analyses of National Health and Nutrition Examination Survey data identified an association between serum Mn and subclinical thyroid changes. The emergence of thyroid deficits as a feature of Mn toxicity suggests that changes in thyroid function may be an underappreciated, but critical, modulator of Mn-induced disease. To better understand the relationship between thyroid function and Mn toxicity, here we further defined the mechanism of Mn-induced hypothyroidism using mouse and rat models. Slc30a10 knockout mice exhibited a profound deficit in thyroid iodine levels that occurred contemporaneously with increases in thyroid Mn levels and preceded the onset of overt hypothyroidism. Wild-type Mn-exposed mice also exhibited increased thyroid Mn levels, an inverse correlation between thyroid Mn and iodine levels, and subclinical hypothyroidism. In contrast, thyroid iodine levels were unaltered in newly generated Slc30a10 knockout rats despite an increase in thyroid Mn levels, and the knockout rats were euthyroid. Thus, Mn-induced thyroid dysfunction in genetic or Mn exposure-induced mouse models occurs due to a reduction in thyroid iodine subsequent to an increase in thyroid Mn levels. Moreover, rat and mouse thyroids have differential sensitivities to Mn, which may impact the manifestations of Mn-induced disease in these routinely used animal models.

Microglial Sp1 induced LRRK2 upregulation in response to manganese exposure, and 17β-estradiol afforded protection against this manganese toxicity

Chronic exposure to elevated levels of manganese (Mn) causes a neurological disorder referred to as manganism, presenting symptoms similar to those of Parkinson’s disease (PD), yet the mechanisms by which Mn induces its neurotoxicity are not completely understood. 17β-estradiol (E2) affords neuroprotection against Mn toxicity in various neural cell types including microglia. Our previous studies have shown that leucine-rich repeat kinase 2 (LRRK2) mediates Mn-induced inflammatory toxicity in microglia. The LRRK2 promoter sequences contain three putative binding sites of the transcription factor (TF), specificity protein 1 (Sp1), which increases LRRK2 promoter activity. In the present study, we tested if the Sp1-LRRK2 pathway plays a role in both Mn toxicity and the protection afforded by E2 against Mn toxicity in BV2 microglial cells. The results showed that Mn induced cytotoxicity, oxidative stress, and tumor necrosis factor-α production, which were attenuated by an LRRK2 inhibitor, GSK2578215A. The overexpression of Sp1 increased LRRK2 promoter activity, mRNA and protein levels, while inhibition of Sp1 with its pharmacological inhibitor, mithramycin A, attenuated the Mn-induced increases in LRRK2 expression. Furthermore, E2 attenuated the Mn-induced Sp1 expression by decreasing the expression of Sp1 via the promotion of the ubiquitin-dependent degradation pathway, which was accompanied by increased protein levels of RING finger protein 4, the E3-ligase of Sp1, Sp1 ubiquitination, and SUMOylation. Taken together, our novel findings suggest that Sp1 serves as a critical TF in Mn-induced LRRK2 expression as well as in the protection afforded by E2 against Mn toxicity through reduction of LRRK2 expression in microglia.

Genome-Wide Identification of OsZIPs in Rice and Gene Expression Analysis under Manganese and Selenium Stress.

Zinc (Zn)- and iron (Fe)-regulating transport-like proteins (ZIPs) are a class of proteins crucial for metal uptake and transport in plants, particularly for Zn and Fe absorption and distribution. These proteins ensure the balance of trace elements essential for plant growth, development, and metabolic activities. However, the role of the rice (Oryza sativa) OsZIP gene family in manganese (Mn) and selenium (Se) transport remains underexplored. This research conducted an all-sided analysis of the rice OsZIPs and identified 16 OsZIP sequences. Phylogenetic analysis categorized the OsZIPs predominantly within the three subfamilies. The expression levels of OsZIPs in rice root and leaf subjected to Mn and Se toxicity stress were examined through quantitative real-time PCR (qRT-PCR). The findings revealed significant differential expression of many OsZIPs under these conditions, indicating a potential regulating effect in the response of rice to Mn and Se toxicity. This work lays a foundation for further functional studies of OsZIPs, enhancing our understanding of the response mechanisms of rice to Mn and Se toxicity and their roles in growth, development, and environmental adaptation.

Regulatory Mechanism through Which Old Soybean Leaves Respond to Mn Toxicity Stress.

Manganese (Mn) is a heavy metal that can cause excessive Mn poisoning in plants, disrupting microstructural homeostasis and impairing growth and development. However, the specific response mechanisms of leaves to Mn poisoning have not been fully elucidated. This study revealed that Mn poisoning of soybean plants resulted in yellowing of old leaves. Physiological assessments of these old leaves revealed significant increases in the antioxidant enzymes activities (peroxidase (POD), superoxide dismutase (SOD), ascorbate peroxidase (APX), and catalase (CAT)) and elevated levels of malondialdehyde (MDA), proline, indoleacetic acid (IAA), and salicylic acid (SA), under 100 μM Mn toxicity. Conversely, the levels of abscisic acid (ABA), gibberellin 3 (GA3), and jasmonic acid (JA) significantly decreased. The Mn content in the affected leaves significantly increased, while the levels of Ca, Na, K, and Cu decreased. Transcriptome analysis revealed 2258 differentially expressed genes in the Mn-stressed leaves, 744 of which were upregulated and 1514 were downregulated; these genes included genes associated with ion transporters, hormone synthesis, and various enzymes. Quantitative RT-PCR (qRT-PCR) verification of fifteen genes confirmed altered gene expression in the Mn-stressed leaves. These findings suggest a complex gene regulatory mechanism under Mn toxicity and stress, providing a foundation for further exploration of Mn tolerance-related gene regulatory mechanisms in soybean leaves. Using the methods described above, this study will investigate the molecular mechanism of old soybean leaves' response to Mn poisoning, identify key genes that play regulatory roles in Mn toxicity stress, and lay the groundwork for cultivating high-quality soybean varieties with Mn toxicity tolerance traits.

A Review on the Impact of Soil Acidification on Plant Nutrient Availability, Crop Productivity, and Management Options in the Ethiopian Highlands

Soil acidity is a type of soil deterioration that has a negative impact on Ethiopia's overall and Western Oromia's specific sustainable agricultural production. Currently, soil acidity in highland portions of Western Oromia, including Gimbi, Nedjo, and surrounding areas, is a major problem that can impede agricultural productivity. Reviewing the mechanisms of soil acidification, which can affect soil nutrient availability and agricultural production, as well as management choices, were done in this context for this review topic. The main causes of acid soils are leaching of exchangeable basic cations and topsoil erosion caused by high temperatures and heavy rains, which promote the loss of organic matter the most. In most of Ethiopia's highland regions, the removal of agricultural waste and ongoing use of inorganic fertilizers that produce acidity are major factors in the development of soil acidity. Al and Mn toxicity are caused by acid soil, which also reduces nutrient availability. Furthermore, agricultural yield decreases due to acidity in the soil. The management options for acid soils include crop types resistant to Al toxicity, liming, and the use of organic materials as integrated forms of soil fertility control. Therefore, lime and organic fertilizers should be employed as crucial agricultural techniques for small-holder farmers in acidic soil locations in order to decrease the effects of soil acidity.

Manganese homeostasis modulates fungal virulence and stress tolerance in Candida albicans.

Transition metals such as manganese provide considerable functionality across biological systems as they are used as cofactors for many catalytic enzymes. The availability of manganese is very limited inside the human body. Consequently, pathogenic microbes have evolved sophisticated mechanisms to uptake this micronutrient inside the human host to sustain their growth and cause infections. Here, we undertook a comprehensive approach to understand how manganese availability impacts the biology of the prevalent fungal pathogen, Candida albicans. We uncovered that manganese homeostasis in this pathogen modulates different biological processes that are essential for host infection which underscores the value of targeting fungal manganese homeostasis for potential antifungal therapeutics development.

Evaluation of Different Agricultural Limes for Bread Wheat and Fababean Production in Acid Soil of West Shewa Zone, Ethiopia

The application of lime is believed to enhance soil health status through improving soil pH, base saturation and reduces Al and Mn toxicities. Liming effects depend on the source, composition, purity and fineness of the lime. The performance of three liming materials and one control treatment was evaluated in a field trial, further evaluation and validation was done at three districts on different farmers’ sites during 2023 main cropping season. The liming materials included calcitic lime, hydrated lime, and quick lime. The treatments laid out in randomized complete block design. The results of the study showed that all tested lime materials (calcitic lime, hydrated lime, and quick lime) improved yield and agronomic performance of wheat, barley and fababean in comparably. This implies that hydrated limes can serve as an alternative agricultural lime to ameliorate soil acidity. Hence, these liming materials can be used as agricultural lime material and the result is confirmed through validation across locations on different testing crops (wheat, barley and Faba bean). So, it is recommended that liming materials which can be easily accessed for the farmers is recommended because of there is no significant difference among liming material tested.

Loss of SLC30A10 manganese transporter alters expression of neurotransmission genes and activates hypoxia-inducible factor signaling in mice.

The essential metal manganese (Mn) induces neuromotor disease at elevated levels. The manganese efflux transporter SLC30A10 regulates brain Mn levels. Homozygous loss-of-function mutations in SLC30A10 induce hereditary Mn neurotoxicity in humans. Our prior characterization of Slc30a10 knockout mice recapitulated the high brain Mn levels and neuromotor deficits reported in humans. But, mechanisms of Mn-induced motor deficits due to SLC30A10 mutations or elevated Mn exposure are unclear. To gain insights into this issue, we characterized changes in gene expression in the basal ganglia, the main brain region targeted by Mn, of Slc30a10 knockout mice using unbiased transcriptomics. Compared with littermates, >1000 genes were upregulated or downregulated in the basal ganglia sub-regions (i.e. caudate putamen, globus pallidus, and substantia nigra) of the knockouts. Pathway analyses revealed notable changes in genes regulating synaptic transmission and neurotransmitter function in the knockouts that may contribute to the motor phenotype. Expression changes in the knockouts were essentially normalized by a reduced Mn chow, establishing that changes were Mn dependent. Upstream regulator analyses identified hypoxia-inducible factor (HIF) signaling, which we recently characterized to be a primary cellular response to elevated Mn, as a critical mediator of the transcriptomic changes in the basal ganglia of the knockout mice. HIF activation was also evident in the liver of the knockout mice. These results: (i) enhance understanding of the pathobiology of Mn-induced motor disease; (ii) identify specific target genes/pathways for future mechanistic analyses; and (iii) independently corroborate the importance of the HIF pathway in Mn homeostasis and toxicity.

Divalent metal content in diet affects severity of manganese toxicity in Drosophila.

Dysregulation of manganese (Mn) homeostasis is a contributing factor in many neuro-degenerative diseases. Adult Drosophila are sensitive to excessive levels of dietary Mn, dying relatively early, and exhibiting biochemical and mobility changes reminiscent of Parkinsonian conditions. To further study Mn homeostasis in Drosophila, we sought to test lower levels of dietary Mn (5 mM) and noted a striking difference in Canton-S adult survivorship on different food. On a cornmeal diet, Mn-treated flies live only about half as long as untreated siblings. Yet, with the same Mn concentration in a molasses diet, adults survive about 80% as long as untreated siblings, and adults raised on a sucrose-yeast diet are completely insensitive to this low dose of dietary Mn. By manipulating metal ion content in the cornmeal diet, and measuring the metal content in each diet, we traced the difference in lifespan to the levels of calcium and magnesium in the food, suggesting that these ions are involved in Mn uptake and/or use. Based on these findings, it is recommended that the total dietary load of metal ions be considered when assessing Mn toxicity.