Mechanisms Of Arsenic Resistance Research Articles

Adaptation to metal(loid)s in strain Mucilaginibacter rubeus P2 involves novel arsenic resistance genes and mechanisms

Arsenic is a ubiquitous environmental toxi substance that affects human health. Compared to inorganic arsenicals, reduced organoarsenicals are more toxic, and some of them are recognized as antibiotics, such as methylarsenite [MAs(III)] and arsinothricin (2-amino-4-(hydroxymethylarsinoyl)butanoate, or AST). To date, organoarsenicals such as MAs(V) and roxarsone [Rox(V)] are still used in agriculture and animal husbandry. How bacteria deal with both inorganic and organoarsenic species is unclear. Recently, we identified an environmental isolate Mucilaginibacter rubeus P2 that has adapted to high arsenic and antinomy levels by triplicating an arsR-mrarsUBact-arsN-arsC-(arsRhp)-hp-acr3-mrme1Bact-mrme2Bactgene cluster. Heterologous expression of mrarsMBact, mrarsUBact, mrme1Bact and mrme2Bact, encoding putative arsenic resistance determinants, in the arsenic hypersensitive strain Escherichia coli AW3110 conferred resistance to As(III), As(V), MAs(III) or Rox(III). Our data suggest that metalloid exposure promotes plasticity in arsenic resistance systems, enhancing host organism adaptation to metalloid stress.

Effect of Arsenic on EPS Synthesis, Biofilm Formation, and Plant Growth-Promoting Abilities of the Endophytes Pseudomonas PD9R and Rahnella laticis PD12R.

Phytoremediation, a cost-effective, eco-friendly alternative to conventional remediation, could expand efforts to remediate arsenic-contaminated soils. As with other pollutants, the plant microbiome may improve phytoremediation outcomes for arsenic-contaminated sites. We used in vitro and in silico methods to compare the arsenic resistance mechanisms, synthesis of extracellular polymeric substances (EPS), biofilm formation, and plant growth-promoting abilities of the endophytes Pseudomonas sp. PD9R and Rahnella laticis PD12R. PD12R, which tolerates arsenate (As(V)) and arsenite (As(III)) to concentrations fivefold greater than PD9R, synthesizes high volumes of EPS in response to arsenic, and sequesters arsenic in the capsular EPS and cells. While arsenic exposure induced EPS synthesis in both strains, only PD12R continued to form biofilms at high As(III) and As(V) concentrations. The effects of endophyte inoculation on Arabidopsis growth varied by strain and As(V) concentration, and PD9R had positive effect on plants exposed to low levels of arsenic. Comparative genomic analyses exploring the EPS synthesis and arsenic resistance mechanisms against other Pseudomonas and Rahnella strains suggest that both strains possess atypical arsenic resistance mechanisms from other plant-associated strains, while the configuration of the EPS synthesis systems appeared to be more broadly distributed among plant- and non-plant-associated strains.

Genome Sequence of Vibrio sp. Strain CCB-PB317, Isolated from a Malaysian Mangrove, and Its Arsenic Resistance Mechanisms.

Vibrio sp. strain CCB-PB317 with potential arsenic detoxification was isolated from a mangrove in Pulau Betong, Malaysia. Here, we report a draft genome sequence of strain CCB-PB317, which comprised 5,157,574 bp with a G+C content of 44.9%. The genome contains genes related to an arsenic resistance system coupled with glycolytic metabolism.

CHARACTERIZATION OF ARSENIC RESISTANT BACTERIA ISOLATED FROM THE SOIL OF KHULNA SHIPYARD

Thirty four arsenic resistant bacterial strains were isolated from the soil samples of Khulna Shipyard. They were isolated by growing them on nutrient broth medium containing 5 mgl-1 of arsenic. From them, five strains were finally selected, and studied their morphological, biochemical and ecological characters in details. They were identified as Bacillus lichenifomis, Bacillus polymyxa, Listeria murrayi, Moraxella urethralis and Planococcus citreus. All of these strains were able to tolerate upto100 ppm (mgl-1) of arsenic (III). It is possibly due to the presence of arsenic (III) resistance mechanism(s) in these bacterial strains. The optimum pH and temperature for the growth of these bacterial strains were 8.5 and 37 °C, respectively.

Comparative Analysis of Arsenic Transport and Tolerance Mechanisms: Evolution from Prokaryote to Higher Plants.

Arsenic (As) is a toxic metalloid for all living organisms and can cause serious harm to humans. Arsenic is also toxic to plants. To alleviate As toxicity, all living organisms (from prokaryotes to higher plants) have evolved comprehensive mechanisms to reduce cytosolic As concentration through the set of As transporters localized at the plasma and tonoplast membranes, which operate either in arsenite As(III) extrusion out of cells (via ArsB, ACR3, and aquaporins) or by sequestering arsenic into vacuoles (by ABC transporters). In addition, a special arsenate resistance mechanism found in some bacterial systems has evolved in an As hyperaccumulating fern Pteris vittata, which involves transforming arsenate As(V) to an As(V) phosphoglycerate derivative by a glyceraldehyde 3-phosphate dehydrogenase and transporting this complex by an efflux transporter. In the present review, we summarize the evolution of these arsenic resistance mechanisms from prokaryotes to eukaryotes and discuss future approaches that could be utilized to better understand and improve As resistance mechanisms in plants.

Arsenic and chromium resistance mechanisms in the Micrococcus luteus group

High arsenic and chromium concentrations are currently receiving attention because of their negative effects on the environment and human health. Microorganisms inhabiting contaminated environments have developed resistance mechanisms against the toxicity of these pollutants. Indeed, members of the bacterial genus Micrococcus have been isolated from different toxic-metal-contaminated environments. However, knowledge concerning the resistance mechanisms of Micrococcus to arsenic and chromium, isolated from contaminated sites, remains scarce. In response, the aim was to examine strains of Micrococcus luteus (An24, Mh, NE2TL6, and NE2TTS4) from the endosphere and soil of two different sites in Mexico contaminated with heavy metals in order to observe any differences in the resistance mechanisms by M. luteus group. The strains were resistant to arsenic (As 3+ , As 5+ ), chromate, dichromate, cobalt, copper, nickel, and zinc. Genome analysis indicated that the heavy metal-resistant strains could be assigned to the M. luteus group ( M. luteus NCTC 2665 T and M. endophyticus JCM 16951 T ), which had more heavy metal-resistant genes (transporters, chaperones, and enzymes) compared to the type strains of the M. luteus group. The bacteria were able to biotransform arsenic (As 3+ and As 5+ ) through a carbon-source-dependent mechanism. The As 5+ was potentially carried out in the cytoplasm through the thioredoxin-dependent pathway, which may be coupled with biosorption. A qualitative analysis of organic acids (OAs) picked up a change in the OA profile that was metal-depending (arsenic or chromium). Our findings on the genome and phenotype tests suggest that the four studied strains of the M. luteus group had developed resistance mechanisms that may have enabled their survival in contaminated sites in Mexico.

Resistance to Arsenite and Arsenate in Saccharomyces cerevisiae Arises through the Subtelomeric Expansion of a Cluster of Yeast Genes.

Arsenic is one of the most prevalent toxic elements in the environment, and its toxicity affects every organism. Arsenic resistance has mainly been observed in microorganisms, and, in bacteria, it has been associated with the presence of the Ars operon. In Saccharomyces cerevisiae, three genes confer arsenic resistance: ARR1, ARR2, and ARR3. Unlike bacteria, in which the presence of the Ars genes confers per se resistance to arsenic, most of the S. cerevisiae isolates present the three ARR genes, regardless of whether the strain is resistant or sensitive to arsenic. To assess the genetic features that make natural S. cerevisiae strains resistant to arsenic, we used a combination of comparative genomic hybridization, whole-genome sequencing, and transcriptomics profiling with microarray analyses. We observed that both the presence and the genomic location of multiple copies of the whole cluster of ARR genes were central to the escape from subtelomeric silencing and the acquisition of resistance to arsenic. As a result of the repositioning, the ARR genes were expressed even in the absence of arsenic. In addition to their relevance in improving our understanding of the mechanism of arsenic resistance in yeast, these results provide evidence for a new cluster of functionally related genes that are independently duplicated and translocated.

A comparative study indicates vertical inheritance and horizontal gene transfer of arsenic resistance-related genes in eukaryotes

Arsenic is a ubiquitous element in the environment, a source of constant evolutionary pressure on organisms. The arsenic resistance machinery is thoroughly described for bacteria. Highly resistant lineages are also common in eukaryotes, but evolutionary knowledge is much more limited. While the origin of the resistance machinery in eukaryotes is loosely attributed to horizontal gene transfer (HGT) from bacteria, only a handful of eukaryotes were deeply studied. Here we investigate the origin and evolution of the core genes in arsenic resistance in eukaryotes using a broad phylogenetic framework. We hypothesize that, as arsenic pressure is constant throughout Earth’s history, resistance mechanisms are probably ancestral to eukaryotes. We identified homologs for each of the arsenic resistance genes in eukaryotes and traced their possible origin using phylogenetic reconstruction. We reveal that: i. an important component of the arsenic-resistant machinery originated before the last eukaryotic common ancestor; ii. later events of gene duplication and HGT generated new homologs that, in many cases, replaced ancestral ones. Even though HGT has an important contribution to the expansion of arsenic metabolism in eukaryotes, we propose the hypothesis of ancestral origin and differential retention of arsenic resistance mechanisms in the group. Key-words: Environmental adaptation; resistance to toxic metalloids; detoxification; comparative genomics; functional phylogenomics.

Arsenic Resistance Mechanisms in Pseudomonas mendocina SMSKVR-3 Strain Isolated from Khetri Copper Mines, Rajasthan, India.

An arsenic resistant bacteria SMSKVR-3 has been isolated from the rhizospheric soil of the metal-contaminated site of khetri copper mines situated in the Jhunjhunu district of Rajasthan, India. The strain showed homology with Pseudomonas mendocina strain ATCC 25411. This gram-negative isolate exhibited optimal growth in M9 minimal media with temperature and salt concentration as 30°C and 0.25% (w/v), respectively, at pH 7.0. The similar growth pattern and SEM analysis of this strain exposed to M9 minimal media alone, M9 media supplemented with 300mM arsenate [As(V)] or M9 media supplemented with 1.34mM arsenite [As(III)] indicate the existence of the strong arsenic resistance mechanism. The isolate was able to produce siderophores and was able to reduce As(V) to As(III). A decrease in polyP concentration from 354.8µg/1010CFUmL-1 at 0h to 0.043µg/1010CFUmL-1 at 8h incubation with As(V) was in correlation with the change in intracellular As(V) concentration (116.98mg L-1/1010 cells at 0h to 88.65mg L-1/1010 at 8h) with time. This shows the possible role of polyP bodies in the regulation of As(V) concentration inside the cell. The presence of arsC gene in P.mendocina SMSKVR-3 was confirmed by the PCR amplification of arsC gene. The BLAST analysis of the sequenced gene represented 98.59% identity with the P. mendocina S5.2 arsenate reductase. These results indicate that the observed arsenic resistance in SMSKVR-3 is due to a combination of siderophore production, the transformation of As(V) to As(III) by arsenate reductase, multi-drug efflux pump, and polyP bodies mediated metal resistance mechanism.

Discerning the role of a functional arsenic-resistance cassette in the evolution and adaptation of a rice pathogen.

Arsenic is highly toxic element to all forms of life and is a major environmental contaminant. Understanding acquisition, detoxification and adaptation mechanisms in bacteria that are associated with the host in arsenic-rich conditions can provide novel insights into the evolutionary dynamics of host–microbe–environment interactions. In the present study, we have investigated an arsenic-resistance mechanism acquired during the evolution of a particular lineage in the population of Xanthomonas oryzae pv. oryzae, which is a serious plant pathogen infecting rice. Our study revealed the horizontal acquisition of a novel chromosomal 12 kb ars cassette in X. oryzae pv. oryzae IXO1088 that confers high resistance to arsenate/arsenite. The ars cassette comprises several genes that constitute an operon induced in the presence of arsenate/arsenite. Transfer of the cloned ars cassette to X. oryzae pv. oryzae BXO512, which lacks the cassette, confers an arsenic-resistance phenotype. Furthermore, the transcriptional response of X. oryzae pv. oryzae IXO1088 under arsenate/arsenite exposure was analysed using RNA sequencing. Arsenic detoxification and efflux, oxidative stress, iron acquisition/storage, and damage repair are the main cellular responses to arsenic exposure. Our investigation has provided insights into the existence of a novel detoxification and adaptation mechanism within the X. oryzae pv. oryzae population to deal with high-arsenic conditions outside the rice plant.

Dependence of arsenic resistance and reduction capacity of Aeromonas hydrophila on carbon substrate

The high toxicity and prevalence of arsenic in the environment have aroused increasing research interest in understanding the mechanisms of microbial arsenic resistance. A wide spectrum of arsenic resistant microbes with ability of arsenic bio-transformation has been isolated from arsenic-contaminated environments. However, arsenic resistance processes and reduction abilities of microbes under various growth conditions remain poorly understood. In this work, a high correlation between the arsenic resistance and reduction ability of Aeromonas hydrophila and the carbon substrate was identified. Genome analysis suggests that the arsenic resistance system is widely present in Aeromonas genus, and the arsenic resistance was associated with the ars operon. The sensitivity of A. hydrophila to As(V) and As(III) depended heavily on the type of carbon substrate. The upregulated expression of arsA, arsB, arsD and/or downregulated expression of glpF might be responsible for the increased microbial tolerance to As(III). The As(V) reduction rate was also affected by the type of carbon substrate. Our results provide new insights into the impacts of carbon substrate on the arsenic biotoxicity as well as arsenic biotransformation processes.

Rhizoglomus intraradices Improves Plant Growth, Root Morphology and Phytohormone Balance of Robinia pseudoacacia in Arsenic-Contaminated Soils

Arbuscular mycorrhizal fungi (AMF) are known to improve the resistance of host plants against various heavy metal stresses. However, the arsenic (As) resistance mechanism of AMF-inoculated woody legumes remains unclear. In this study, black locust (Robinia pseudoacacia L.) seedlings were cultivated in potted soils inoculated with or without AMF Rhizoglomus intraradices under three different levels of As stress (0, 100, and 200 mg As kg–1 soil) over 4 months. The objective of this paper was to investigate the effects of AMF on plant growth, root morphology, and the content and ratio of endogenous phytohormones and soil glomalin under As stress condition. As stress toxicity suppressed the AM spore germination and colonization, plant growth, and the content of soil glomalin and changed the morphological characteristics of the roots and the balance of endogenous hormone levels in plants. However, R. intraradices inoculation improved the shoot and root dry weights, total root length, root surface area, root volume, and the number of root forks and tips across all As treatments. R. intraradices inoculation obviously decreased the percentage of root length in the 0- to 0.2-mm diameter class and increased those in the 0.5- to 1.0-mm and >1.0-mm diameter classes; the percentages in the 0.2- to 0.5-mm diameter class were less affected by R. intraradices inoculation. The concentrations of the easily extractable glomalin-related (EE-GRSP) and total glomalin-related soil protein (T-GRSP) were higher in the of R. intraradices-inoculated seedlings than those in the non-inoculated seedlings. Furthermore, R. intraradices inoculation increased the concentrations of indole-3-acetic acid (IAA) and abscisic acid (ABA), but decreased the concentrations of gibberellic acid (GA) and zeatin riboside (ZR). The phytohormone ratios of IAA/ABA, GA/ABA, ZR/ABA, and (IAA + GA + ZR)/IAA in the R. intraradices-inoculated seedlings were lower than those in the non-inoculated seedlings. These results indicated that R. intraradices alleviated As toxicity in R. pseudoacacia seedlings by improving their plant growth, altering root morphology, regulating the concentrations and ratios of phytohormones, and increasing the concentration of soil glomalin. The results suggested that AMF-inoculated R. pseudoacacia seedlings would be a critical factor in successful vegetation restoration and soil development in As-contaminated soils.

Identification of Resistance Genes and Response to Arsenic in Rhodococcus aetherivorans BCP1.

Arsenic (As) ranks among the priority metal(loid)s that are of public health concern. In the environment, arsenic is present in different forms, organic or inorganic, featured by various toxicity levels. Bacteria have developed different strategies to deal with this toxicity involving different resistance genetic determinants. Bacterial strains of Rhodococcus genus, and more in general Actinobacteria phylum, have the ability to cope with high concentrations of toxic metalloids, although little is known on the molecular and genetic bases of these metabolic features. Here we show that Rhodococcus aetherivorans BCP1, an extremophilic actinobacterial strain able to tolerate high concentrations of organic solvents and toxic metalloids, can grow in the presence of high concentrations of As(V) (up to 240 mM) under aerobic growth conditions using glucose as sole carbon and energy source. Notably, BCP1 cells improved their growth performance as well as their capacity of reducing As(V) into As(III) when the concentration of As(V) is within 30–100 mM As(V). Genomic analysis of BCP1 compared to other actinobacterial strains revealed the presence of three gene clusters responsible for organic and inorganic arsenic resistance. In particular, two adjacent and divergently oriented ars gene clusters include three arsenate reductase genes (arsC1/2/3) involved in resistance mechanisms against As(V). A sequence similarity network (SSN) and phylogenetic analysis of these arsenate reductase genes indicated that two of them (ArsC2/3) are functionally related to thioredoxin (Trx)/thioredoxin reductase (TrxR)-dependent class and one of them (ArsC1) to the mycothiol (MSH)/mycoredoxin (Mrx)-dependent class. A targeted transcriptomic analysis performed by RT-qPCR indicated that the arsenate reductase genes as well as other genes included in the ars gene cluster (possible regulator gene, arsR, and arsenite extrusion genes, arsA, acr3, and arsD) are transcriptionally induced when BCP1 cells were exposed to As(V) supplied at two different sub-lethal concentrations. This work provides for the first time insights into the arsenic resistance mechanisms of a Rhodococcus strain, revealing some of the unique metabolic requirements for the environmental persistence of this bacterial genus and its possible use in bioremediation procedures of toxic metal contaminated sites.

Six New Families of Aerobic Arsenate Reducing Bacteria: Leclercia, Raoultella, Kosakonia, Lelliottia, Yokenella, and Kluyvera

Elevated levels of arsenate can occur in the environment due to processes such as mining activities, and microbes must utilize various detoxification mechanisms to adapt to the associated pressure. The aim of this study was to identify as many aerobic arsenate-reducing bacteria (aARB) as possible in order to investigate their phylogenetic diversity and molecular mechanisms of arsenic resistance. We isolated 24 strains of aARB from a long-standing arsenic contaminated environment and detected the ars genotype in them. All 24 strains could reduce approximately 90% of arsenate, and 23 of them exhibited (6–59%) arsenic removal ability. The 16S rRNA gene analyses revealed aARB representing 16 genera were abundant. The included six genera, namely Leclercia, Raoultella, Kosakonia, Lelliottia, Yokenella, and Kluyvera, that were not previously known to reduce or exhibit resistance to arsenic. Twenty-one of 24 aARB were positive for ars amplification and 17 of them harbored a putative arsC gene, which is well-known for its involvement in arsenate reduction. However, the arsenic resistance associated with aARB strains is not always determined by the ars operon system. These results have provided additional insight into aARB and their potential for arsenic transformation and bioremediation.

Transcriptome analysis of silver, palladium, and selenium stresses in Pantoea sp. IMH

Heavy metal contamination is a significant environmental issue. Using bacteria for removal and reduction of heavy metals is an attractive alternative owing to its low-cost and eco-friendly properties. However, the mechanisms of resistance to and reduction of Ag(I), Pd(II), and Se(IV), especially in the same strain, remain unclear. Here, Pantoea sp. IMH was examed for its reduction of Ag(I), Pd(II), and Se(IV) to nanoparticles (NPs), and the molecular mechanism was investigated by transcriptome analysis. The results revealed that genes encoding binding, transport, catalytic activity, and metabolism were differentially expressed in cells exposed to Ag(I), Pd(II), and Se(IV). The same resistance mechanisms for all metals included multiple stress resistance protein BhsA and glutathione detoxification metabolism. However, zinc transport protein and sulfate metabolism played an important role in the resistance to cationic metals (Ag+ and Pd2+), while the oxalate transporter and arsenic resistance mechanisms were specifically involved in the resistance to and reduction of anion (SeO32−). In addition, Ag(I) was speculated to be reduced to AgNPs by glucose and cytochrome CpxP was involved in Pd(II) reduction. Our results provided new clues on the mechanisms of resistance to and reduction of Ag(I), Pd(II), and Se(IV).

Characterization of a promiscuous cadmium and arsenic resistance mechanism in Thermus thermophilus HB27 and potential application of a novel bioreporter system

BackgroundThe characterization of the molecular determinants of metal resistance has potential biotechnological application in biosensing and bioremediation. In this context, the bacterium Thermus thermophilus HB27 is a metal tolerant thermophile containing a set of genes involved in arsenic resistance which, differently from other microbes, are not organized into a single operon. They encode the proteins: arsenate reductase, TtArsC, arsenic efflux membrane transporter, TtArsX, and transcriptional repressor, TtSmtB.ResultsIn this work we show that the arsenic efflux protein TtArsX and the arsenic responsive transcriptional repressor TtSmtB are required to provide resistance to cadmium. We analyzed the sensitivity to Cd(II) of mutants lacking TtArsX, finding that they are more sensitive to this metal than the wild type strain. In addition, using promoter probe reporter plasmids, we show that the transcription of TtarsX is also stimulated by the presence of Cd(II) in a TtSmtB-dependent way. Actually, a regulatory circuit composed of TtSmtB and a reporter gene expressed from the TtarsX promoter responds to variation in Cd(II), As(III) and As(V) concentrations.ConclusionsOur results demonstrate that the system composed by TtSmtB and TtArsX is responsible for both the arsenic and cadmium resistance in T. thermophilus. The data also support the use of T. thermophilus as a suitable chassis for the design and development of As-Cd biosensors.

Signature Arsenic Detoxification Pathways in Halomonas sp. Strain GFAJ-1.

ABSTRACTSince the original report that Halomonas sp. strain GFAJ-1 was capable of using arsenic instead of phosphorus to sustain growth, additional studies have been conducted, and GFAJ-1 is now considered a highly arsenic-resistant but phosphorus-dependent bacterium. However, the mechanisms supporting the extreme arsenic resistance of the GFAJ-1 strain remain unknown. In this study, we show that GFAJ-1 has multiple distinct arsenic resistance mechanisms. It lacks the genes to reduce arsenate, which is the essential step in the well-characterized resistance mechanism of arsenate reduction coupled to arsenite extrusion. Instead, GFAJ-1 has two arsenic resistance operons, arsH1-acr3-2-arsH2 and mfs1-mfs2-gapdh, enabling tolerance to high levels of arsenate. mfs2 and gapdh encode proteins homologous to Pseudomonas aeruginosa ArsJ and glyceraldehyde-3-phosphate dehydrogenase (GAPDH), respectively, which constitute the equivalent of an As(V) efflux system to catalyze the transformation of inorganic arsenate to pentavalent organoarsenical 1-arseno-3-phosphoglycerate and its subsequent extrusion. Surprisingly, the arsH1-acr3-2-arsH2 operon seems to consist of typical arsenite resistance genes, but this operon is sufficient to confer both arsenite and arsenate resistance on Escherichia coli AW3110 even in the absence of arsenate reductase, suggesting a novel pathway of arsenic detoxification. The simultaneous occurrence of these two unusual detoxification mechanisms enables the adaptation of strain GFAJ-1 to the particularly arsenic-rich environment of Mono Lake.

Mechanism of arsenic resistance in endophytic bacteria isolated from endemic plant of mine tailings and their arsenophore production.

Arsenic contamination is an important environmental problem around the world since its high toxicity, and bacteria resist to this element serve as valuable resource for its bioremediation. Aiming at searching the arsenic-resistant bacteria and determining their resistant mechanism, a total of 27 strains isolated from roots of Prosopis laevigata and Spharealcea angustifolia grown in a heavy metal-contaminated region in Mexico were investigated. The minimum inhibitory concentration (MIC) and transformation abilities of arsenate (As5+) and arsenite (As3+), arsenophore synthesis, arsenate uptake, and cytoplasmatic arsenate reductase (arsC), and arsenite transporter (arsB) genes were studied for these strains. Based on these results and the 16S rDNA sequence analysis, these isolates were identified as arsenic-resistant endophytic bacteria (AREB) belonging to the genera Arthrobacter, Bacillus, Brevibacterium, Kocuria, Microbacterium, Micrococcus, Pseudomonas, and Staphylococcus. They could tolerate high concentrations of arsenic with MIC from 20 to > 100mM for As5+ and 10-20mM for As3+. Eleven isolates presented dual abilities of As5+ reduction and As3+ oxidation. As the most effective strains, Micrococcus luteus NE2E1 reduced 94% of the As5+ and Pseudomonas zhaodongensis NM2E7 oxidized 46% of As3+ under aerobic condition. About 70 and 44% of the test strains produced arsenophores to chelate As5+ and As3+, respectively. The AREB may absorb arsenate via the same receptor of phosphate uptake or via other way in some case. The cytoplasmic arsenate reductase and alternative arsenate reduction pathways exist in these AREB. Therefore, these AREB could be candidates for the bioremediation process.

Draft Genome Sequence of Arsenic-Resistant Microbacterium sp. Strain SZ1 Isolated from Arsenic-Bearing Gold Ores.

ABSTRACTMicrobacterium sp. strain SZ1 isolated from gold ores of a Malaysia gold mine was found to be highly resistant to arsenic. Here, we report the draft genome sequence of SZ1, which may provide further insights into understanding its arsenic resistance mechanism. In this draft genome, a complete set of ars operons and two additional scattered ars genes were encoded.

Structural studies of the ArsD arsenic metallochaperone using molecular dynamics

Over the past three decades the occurrence of high environmental concentrations of arsenic has been recognized as a major public health concern. Arsenic is a carcinogen and causative agent for number of diseases. The toxic and carcinogenic effects of arsenic are the result of inactivation of specific enzymes of metabolism, induction of oxidative stress, inhibition of DNA repair mechanisms and deregulation of cell proliferation. Despite its toxicity, arsenic has a long history of usage as chemotherapeutic agent. Today, drugs containing arsenic (and the related metalloid antimony) are used for treating acute promyelocytic leukemia and diseases caused by protozoan parasites. In response to its toxicity, many microorganisms have developed arsenic resistance mechanism. In bacteria, arsenic resistance genes are organized in ars operons. The best characterized, the ars operon from Escherichia coli plasmid R773, has five genes, arsRDABC. ArsC is a reductase that reduces inorganic As(V) to As(III). ArsR is a 117-residue homodimeric As(III)-responsive transcriptional repressor with high affinity for the ars promoter. ArsA is an ATPase, which is the catalytic subunit of the ArsAB efflux pump, and ArsD is an As(III) chaperone to the ArsAB pump. ArsD is a homodimer of two 120-residue subunits with three vicinal cysteine pairs, Cys12-Cys13, Cys112-Cys113 and Cys119-Cys120. A fully-active truncated version of ArsD protein with 109 residues (ArsD109) has been crystallized, and the structure has been solved using X-ray crystallography. Biochemical studies suggested that wild-type ArsD binds three As(III) per monomer, while the derivative with a truncation at residue 109 binds only a single As(III). To understand the secondary structure and folding of the C-terminus of ArsD, which includes two cysteine pairs Cys112-Cys113 and Cys119-Cys120, Molecular Dynamics (MD) simulations were employed using AMBER software in presence or absence of arsenite [As(III)] ligand.