Bacterial transformations of and resistances to heavy metals. - Related Documents




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13701.0000Bacterial transformations of and resistances to heavy metals. Bacteria carry out chemical transformations of heavy metals. These transformations (including oxidation, reduction, methylation, and demethylation) are sometimes byproducts of normal metabolism and confer no known advantage upon the organism responsible. Sometimes, however, the transformations constitute a mechanism of resistance. Many species of bacteria have genes that control resistances to specific toxic heavy metals. These resistances often are determined by extrachromosomal DNA molecules (plasmids). The same mechanisms of resistance occur in bacteria from soil, water, industrial waste, and clinical sources. The mechanism of mercury and organomercurial resistance is the enzymatic detoxification of the mercurials into volatile species (methane, ethane, metallic HgO) which are rapidly lost from the environment. Cadmium and arsenate resistances are due to reduced net accumulation of these toxic materials. Efficient efflux pumps cause the rapid excretion of Cd2+ and AsO4(3-). The mechanisms of arsenite and of antimony resistance, usually found associated with arsenate resistance, are not known. Silver resistance is due to lowered affinity of the cells for Ag+, which can be complexed with extracellular halides, thiols, or organic compounds. Sensitivity is due to binding of Ag+ more effectively to cells than to Cl-.19846367730
932210.9997Copper uptake and resistance in bacteria. Copper ions are essential for bacteria but can cause a number of toxic cellular effects if levels of free ions are not controlled. Investigations of copper-resistant bacteria have revealed several mechanisms, mostly plasmid-determined, that prevent cellular uptake of high levels of free copper ions. However, these studies have also revealed that bacteria apparently have efficient chromosomally encoded systems for uptake and management of trace levels of copper. This review will explore the relationship of copper uptake systems to resistance mechanisms and the possibility that copper resistance has evolved directly through modification of chromosomal copper uptake genes.19938437513
13520.9997Resistance to arsenic compounds in microorganisms. Arsenic ions, frequently present as environmental pollutants, are very toxic for most microorganisms. Some microbial strains possess genetic determinants that confer resistance. In bacteria, these determinants are often found on plasmids, which has facilitated their study at the molecular level. Bacterial plasmids conferring arsenic resistance encode specific efflux pumps able to extrude arsenic from the cell cytoplasm thus lowering the intracellular concentration of the toxic ions. In Gram-negative bacteria, the efflux pump consists of a two-component ATPase complex. ArsA is the ATPase subunit and is associated with an integral membrane subunit, ArsB. Arsenate is enzymatically reduced to arsenite (the substrate of ArsB and the activator of ArsA) by the small cytoplasmic ArsC polypeptide. In Gram-positive bacteria, comparable arsB and arsC genes (and proteins) are found, but arsA is missing. In addition to the wide spread plasmid arsenic resistance determinant, a few bacteria confer resistance to arsenite with a separate determinant for enzymatic oxidation of more-toxic arsenite to less-toxic arsenate. In contrast to the detailed information on the mechanisms of arsenic resistance in bacteria, little work has been reported on this subject in algae and fungi.19947848659
932330.9997Metal resistance and accumulation in bacteria. Recent research on the ecology, physiology and genetics of metal resistance and accumulation in bacteria has significantly increased the basic understanding of microbiology in these areas. Research has clearly demonstrated the versatility of bacteria to cope with toxic metal ions. For example, certain strains of bacteria can efficiently efflux toxic ions such as cadmium, that normally exert an inhibitory effect on bacteria. Some bacteria such as Escherichia coli and Staphylococcus sp. can volatilize mercury via enzymatic transformations. It is also noteworthy that many of these resistance mechanisms are encoded on plasmids or transposons. By expanding the knowledge on metal-resistance and accumulation mechanisms in bacteria, it may be possible to utilize certain strains to recover precious metals such as gold and silver, or alternatively remove toxic metal ions from environments or products where their presence is undesirable.198714543146
869540.9996Cadmium transport, resistance, and toxicity in bacteria, algae, and fungi. Cadmium is an important environmental pollutant and a potent toxicant to bacteria, algae, and fungi. Mechanisms of Cd toxicity and resistance are variable, depending on the organism. It is very clear that the form of the metal and the environment it is studied in, play an important role in how Cd exerts its effect and how the organism(s) responds. A wide range of Cd concentrations have been used to designate resistance in organisms. To date, no concentration has been specified that is applicable to all species studied under standardized conditions. Cadmium exerts its toxic effect(s) over a wide range of concentrations. In most cases, algae and cyanobacteria are the most sensitive organisms, whereas bacteria and fungi appear to be more resistant. In some bacteria, plasmid-encoded resistance can lead to reduced Cd2+ uptake. However, some Gram-negative bacteria without plasmids are just as resistant to Cd as are bacteria containing plasmids encoding for Cd resistance. According to Silver and Misra (1984), there is no evidence for enzymatic or chemical transformations associated with Cd resistance. Insufficient information is available on the genetics of Cd uptake and resistance in cyanobacteria and algae. Mechanisms remain largely unknown at this point in time. Cadmium is toxic to these organisms, causing severe inhibition of such physiological processes as growth, photosynthesis, and nitrogen fixation at concentrations less than 2 ppm, and often in the ppb range (Tables 2 and 3). Cadmium also causes pronounced morphological aberrations in these organisms, which are probably related to deleterious effects on cell division. This may be direct or indirect, as a result of Cd effects on protein synthesis and cellular organelles such as mitochondria and chloroplasts. Cadmium is accumulated internally in algae (Table 4) as a result of a two-phase uptake process. The first phase involves a rapid physicochemical adsorption of Cd onto cell wall binding sites, which are probably proteins and (or) polysaccharides. This is followed by a lag period and then a slow, steady intracellular uptake. This latter phase is energy dependent and may involve transport systems used to accumulate other divalent cations, such as Mn2+ and Ca2+. Some data indicate that Cd resistance, and possibly uptake, in algae and cyanobacteria is controlled by a plasmid-encoded gene(s). Although considerable information is available on Cd toxicity to, and uptake in fungi, further work is clearly needed in several areas. There is little information about Cd uptake by filamentous fungi, and even in yeasts, information on the specificity, kinetics, and mechanisms of Cd uptake is limited.(ABSTRACT TRUNCATED AT 400 WORDS)19863089567
869050.9996Cellular and genetic mechanism of bacterial mercury resistance and their role in biogeochemistry and bioremediation. Mercury (Hg) is a highly toxic element that occurs at low concentrations in nature. However, various anthropogenic and natural sources contribute around 5000 to 8000 metric tons of Hg per year, rapidly deteriorating the environmental conditions. Mercury-resistant bacteria that possess the mer operon system have the potential for Hg bioremediation through volatilization from the contaminated milieus. Thus, bacterial mer operon plays a crucial role in Hg biogeochemistry and bioremediation by converting both reactive inorganic and organic forms of Hg to relatively inert, volatile, and monoatomic forms. Both the broad-spectrum and narrow-spectrum bacteria harbor many genes of mer operon with their unique definitive functions. The presence of mer genes or proteins can regulate the fate of Hg in the biogeochemical cycle in the environment. The efficiency of Hg transformation depends upon the nature and diversity of mer genes present in mercury-resistant bacteria. Additionally, the bacterial cellular mechanism of Hg resistance involves reduced Hg uptake, extracellular sequestration, and bioaccumulation. The presence of unique physiological properties in a specific group of mercury-resistant bacteria enhances their bioremediation capabilities. Many advanced biotechnological tools also can improve the bioremediation efficiency of mercury-resistant bacteria to achieve Hg bioremediation.202234464861
932160.9996Copper resistance determinants in bacteria. Copper is an essential trace element that is utilized in a number of oxygenases and electron transport proteins, but it is also a highly toxic heavy metal, against which all organisms must protect themselves. Known bacterial determinants of copper resistance are plasmid-encoded. The mechanisms which confer resistance must be integrated with the normal metabolism of copper. Different bacteria have adopted diverse strategies for copper resistance, and this review outlines what is known about bacterial copper resistance mechanisms and their genetic regulation.19921741459
931970.9996A role for copper in protozoan grazing - two billion years selecting for bacterial copper resistance. The Great Oxidation Event resulted in integration of soft metals in a wide range of biochemical processes including, in our opinion, killing of bacteria by protozoa. Compared to pressure from anthropologic copper contamination, little is known on impacts of protozoan predation on maintenance of copper resistance determinants in bacteria. To evaluate the role of copper and other soft metals in predatory mechanisms of protozoa, we examined survival of bacteria mutated in different transition metal efflux or uptake systems in the social amoeba Dictyostelium discoideum. Our data demonstrated a strong correlation between the presence of copper/zinc efflux as well as iron/manganese uptake, and bacterial survival in amoebae. The growth of protozoa, in turn, was dependent on bacterial copper sensitivity. The phagocytosis of bacteria induced upregulation of Dictyostelium genes encoding the copper uptake transporter p80 and a triad of Cu(I)-translocating P(IB) -type ATPases. Accumulated Cu(I) in Dictyostelium was monitored using a copper biosensor bacterial strain. Altogether, our data demonstrate that Cu(I) is ultimately involved in protozoan predation of bacteria, supporting our hypothesis that protozoan grazing selected for the presence of copper resistance determinants for about two billion years.201627528008
13680.9995Operon mer: bacterial resistance to mercury and potential for bioremediation of contaminated environments. Mercury is present in the environment as a result of natural processes and from anthropogenic sources. The amount of mercury mobilized and released into the biosphere has increased since the beginning of the industrial age. Generally, mercury accumulates upwards through aquatic food chains, so that organisms at higher trophic levels have higher mercury concentrations. Some bacteria are able to resist heavy metal contamination through chemical transformation by reduction, oxidation, methylation and demethylation. One of the best understood biological systems for detoxifying organometallic or inorganic compounds involves the mer operon. The mer determinants, RTPCDAB, in these bacteria are often located in plasmids or transposons and can also be found in chromosomes. There are two classes of mercury resistance: narrow-spectrum specifies resistance to inorganic mercury, while broad-spectrum includes resistance to organomercurials, encoded by the gene merB. The regulatory gene merR is transcribed from a promoter that is divergently oriented from the promoter for the other mer genes. MerR regulates the expression of the structural genes of the operon in both a positive and a negative fashion. Resistance is due to Hg2+ being taken up into the cell and delivered to the NADPH-dependent flavoenzyme mercuric reductase, which catalyzes the two-electron reduction of Hg2+ to volatile, low-toxicity Hg0. The potential for bioremediation applications of the microbial mer operon has been long recognized; consequently, Escherichia coli and other wild and genetically engineered organisms for the bioremediation of Hg2+-contaminated environments have been assayed by several laboratories.200312917805
869190.9995Genetic basis and importance of metal resistant genes in bacteria for bioremediation of contaminated environments with toxic metal pollutants. Metal pollution is one of the most persistent and complex environmental issues, causing threat to the ecosystem and human health. On exposure to several toxic metals such as arsenic, cadmium, chromium, copper, lead, and mercury, several bacteria has evolved with many metal-resistant genes as a means of their adaptation. These genes can be further exploited for bioremediation of the metal-contaminated environments. Many operon-clustered metal-resistant genes such as cadB, chrA, copAB, pbrA, merA, and NiCoT have been reported in bacterial systems for cadmium, chromium, copper, lead, mercury, and nickel resistance and detoxification, respectively. The field of environmental bioremediation has been ameliorated by exploiting diverse bacterial detoxification genes. Genetic engineering integrated with bioremediation assists in manipulation of bacterial genome which can enhance toxic metal detoxification that is not usually performed by normal bacteria. These techniques include genetic engineering with single genes or operons, pathway construction, and alternations of the sequences of existing genes. However, numerous facets of bacterial novel metal-resistant genes are yet to be explored for application in microbial bioremediation practices. This review describes the role of bacteria and their adaptive mechanisms for toxic metal detoxification and restoration of contaminated sites.201626860944
138100.9995Resistance mechanisms to arsenicals and antimonials. Salts and organic derivatives of arsenic and antimony are quite toxic. Living organisms have adapted to this toxicity by the evolution of resistance mechanisms. Both prokaryotic and eukaryotic cells develop resistance when exposed to arsenicals or antimonials. In the case of bacteria resistance is conferred by plasmid-encoded arsenical resistance (ars) operons. The genes and gene products of the ars operon of the clinically-isolated conjugative R-factor R773 have been identified and their mechanism of action elucidated. The operon encodes an ATP-driven pump that extrudes arsenite and antimonite from the cells. The lowering of their intracellular concentration results in resistance. Arsenate resistance results from the action of the plasmid-encoded arsenate reductase that reduces arsenate to arsenite, which is then pumped out of the cell.19958852270
167110.9995Ion efflux systems involved in bacterial metal resistances. Studying metal ion resistance gives us important insights into environmental processes and provides an understanding of basic living processes. This review concentrates on bacterial efflux systems for inorganic metal cations and anions, which have generally been found as resistance systems from bacteria isolated from metal-polluted environments. The protein products of the genes involved are sometimes prototypes of new families of proteins or of important new branches of known families. Sometimes, a group of related proteins (and presumedly the underlying physiological function) has still to be defined. For example, the efflux of the inorganic metal anion arsenite is mediated by a membrane protein which functions alone in Gram-positive bacteria, but which requires an additional ATPase subunit in some Gram-negative bacteria. Resistance to Cd2+ and Zn2+ in Gram-positive bacteria is the result of a P-type efflux ATPase which is related to the copper transport P-type ATPases of bacteria and humans (defective in the human hereditary diseases Menkes' syndrome and Wilson's disease). In contrast, resistance to Zn2+, Ni2+, Co2+ and Cd2+ in Gram-negative bacteria is based on the action of proton-cation antiporters, members of a newly-recognized protein family that has been implicated in diverse functions such as metal resistance/nodulation of legumes/cell division (therefore, the family is called RND). Another new protein family, named CDF for 'cation diffusion facilitator' has as prototype the protein CzcD, which is a regulatory component of a cobalt-zinc-cadmium resistance determinant in the Gram-negative bacterium Alcaligenes eutrophus. A family for the ChrA chromate resistance system in Gram-negative bacteria has still to be defined.19957766211
9327120.9995Detection of the merA gene and its expression in the environment. Bacterial transformation of mercury in the environment has received much attention owing to the toxicity of both the ionic form and organomercurial compounds. Bacterial resistance to mercury and the role of bacteria in mercury cycling have been widely studied. The genes specifying the required functions for resistance to mercury are organized on the mer operon. Gene probing methodologies have been used for several years to detect specific gene sequences in the environment that are homologous to cloned mer genes. While mer genes have been detected in a wide variety of environments, less is known about the expression of these genes under environmental conditions. We combined new methodologies for recovering specific gene mRNA transcripts and mercury detection with a previously described method for determining biological potential for mercury volatilization to examine the effect of mercury concentrations and nutrient availability on rates of mercury volatilization and merA transcription. Levels of merA-specific transcripts and Hg(II) volatilization were influenced more by microbial activity (as manipulated by nutrient additions) than by the concentration of total mercury. The detection of merA-specific transcripts in some samples that did not reduce Hg(II) suggests that rates of mercury volatilization in the environment may not always be proportional to merA transcription.19968849424
9320130.9995Bacterial resistance to arsenic protects against protist killing. Protists kill their bacterial prey using toxic metals such as copper. Here we hypothesize that the metalloid arsenic has a similar role. To test this hypothesis, we examined intracellular survival of Escherichia coli (E. coli) in the amoeba Dictyostelium discoideum (D. discoideum). Deletion of the E. coli ars operon led to significantly lower intracellular survival compared to wild type E. coli. This suggests that protists use arsenic to poison bacterial cells in the phagosome, similar to their use of copper. In response to copper and arsenic poisoning by protists, there is selection for acquisition of arsenic and copper resistance genes in the bacterial prey to avoid killing. In agreement with this hypothesis, both copper and arsenic resistance determinants are widespread in many bacterial taxa and environments, and they are often found together on plasmids. A role for heavy metals and arsenic in the ancient predator-prey relationship between protists and bacteria could explain the widespread presence of metal resistance determinants in pristine environments.201728210928
177140.9995Bacterial mercury resistance from atoms to ecosystems. Bacterial resistance to inorganic and organic mercury compounds (HgR) is one of the most widely observed phenotypes in eubacteria. Loci conferring HgR in Gram-positive or Gram-negative bacteria typically have at minimum a mercuric reductase enzyme (MerA) that reduces reactive ionic Hg(II) to volatile, relatively inert, monoatomic Hg(0) vapor and a membrane-bound protein (MerT) for uptake of Hg(II) arranged in an operon under control of MerR, a novel metal-responsive regulator. Many HgR loci encode an additional enzyme, MerB, that degrades organomercurials by protonolysis, and one or more additional proteins apparently involved in transport. Genes conferring HgR occur on chromosomes, plasmids, and transposons and their operon arrangements can be quite diverse, frequently involving duplications of the above noted structural genes, several of which are modular themselves. How this very mobile and plastic suite of proteins protects host cells from this pervasive toxic metal, what roles it has in the biogeochemical cycling of Hg, and how it has been employed in ameliorating environmental contamination are the subjects of this review.200312829275
134150.9995Bacterial tellurite resistance. Tellurium compounds are used in several industrial processes, although they are relatively rare in the environment. Genes associated with tellurite resistance (TeR) are found in many pathogenic bacteria. Tellurite can be detoxified through interactions with cellular thiols, such as glutathione, or a methyltransferase-catalyzed reaction, although neither process appears involved in plasmid-mediated TeR.199910203839
8692160.9995Genetic mechanisms of arsenic detoxification and metabolism in bacteria. Arsenic, distributed pervasively in the natural environment, is an extremely toxic substance which can severely impair the normal functions of living cells. Research on the genetic mechanisms of arsenic metabolism is of great importance for remediating arsenic-contaminated environments. Many organisms, including bacteria, have developed various strategies to tolerate arsenic, by either detoxifying this harmful element or utilizing it for energy generation. This review summarizes arsenic detoxification as well as arsenic respiratory metabolic pathways in bacteria and discusses novel arsenic resistance pathways in various bacterial strains. This knowledge provides insights into the mechanisms of arsenic biotransformation in bacteria. Multiple detoxification strategies among bacteria imply possible functional relationships among different arsenic detoxification/metabolism pathways. In addition, this review sheds light on the bioremediation of arsenic-contaminated environments and prevention of antibiotic resistance.201930349994
9328170.9994Man-made cell-like compartments for molecular evolution. Cellular compartmentalization is vital for the evolution of all living organisms. Cells keep together the genes, the RNAs and proteins that they encode, and the products of their activities, thus linking genotype to phenotype. We have reproduced this linkage in the test tube by transcribing and translating single genes in the aqueous compartments of water-in-oil emulsions. These compartments, with volumes close to those of bacteria, can be recruited to select genes encoding catalysts. A protein or RNA with a desired catalytic activity converts a substrate attached to the gene that encodes it to product. In other compartments, substrates attached to genes that do not encode catalysts remain unmodified. Subsequently, genes encoding catalysts are selectively enriched by virtue of their linkage to the product. We demonstrate the linkage of genotype to phenotype in man-made compartments using a model system. A selection for target-specific DNA methylation was based on the resistance of the product (methylated DNA) to restriction digestion. Genes encoding HaeIII methyltransferase were selected from a 10(7)-fold excess of genes encoding another enzyme.19989661199
8632180.9994Microbial interactions in the arsenic cycle: adoptive strategies and applications in environmental management. Arsenic (As) is a nonessential element that is often present in plants and in other organisms. However, it is one of the most hazardous of toxic elements globally. In many parts of the world, arsenic contamination in groundwater is a serious and continuing threat to human health. Microbes play an important role in regulating the environmental fate of arsenic. Different microbial processes influence the biogeochemical cycling of arsenic in ways that affect the accumulation of different arsenic species in various ecosystem compartments. For example, in soil, there are bacteria that methylate arsenite to trimethylarsine gas, thereby releasing arsenic to the atmosphere.In marine ecosystems, microbes exist that can convert inorganic arsenicals to organic arsenicals (e.g., di- and tri-methylated arsenic derivatives, arsenocholine,arsenobetaine, arsenosugars, arsenolipids). The organo arsenicals are further metabolized to complete the arsenic cycle.Microbes have developed various strategies that enable them to tolerate arsenic and to survive in arsenic-rich environments. Such strategies include As exclusion from cells by establishing permeability barrier, intra- and extracellular sequestration,active efflux pumps, enzymatic reduction, and reduction in the sensitivity of cellular targets. These strategies are used either singly or in combination. In bacteria,the genes for arsenic resistance/detoxification are encoded by the arsenic resistance operons (ars operon).In this review, we have addressed and emphasized the impact of different microbial processes (e.g., arsenite oxidation, cytoplasmic arsenate reduction, respiratory arsenate reduction, arsenite methylation) on the arsenic cycle. Microbes are the only life forms reported to exist in heavy arsenic-contaminated environments. Therefore,an understanding of the strategies adopted by microbes to cope with arsenic stress is important in managing such arsenic-contaminated sites. Further future insights into the different microbial genes/proteins that are involved in arsenic resistance may also be useful for developing arsenic resistant crop plants.201323232917
761190.9994Copper-responsive gene regulation in bacteria. Copper is an essential cofactor of various enzymes, but free copper is highly toxic to living cells. To maintain cellular metabolism at different ambient copper concentrations, bacteria have evolved specific copper homeostasis systems that mostly act as defence mechanisms. As well as under free-living conditions, copper defence is critical for virulence in pathogenic bacteria. Most bacteria synthesize P-type copper export ATPases as principal defence determinants when copper concentrations exceed favourable levels. In addition, many bacteria utilize resistance-nodulation-cell division (RND)-type efflux systems and multicopper oxidases to cope with excess copper. This review summarizes our current knowledge on copper-sensing transcriptional regulators, which we assign to nine different classes. Widespread one-component regulators are CueR, CopY and CsoR, which were initially identified in Escherichia coli, Enterococcus hirae and Mycobacterium tuberculosis, respectively. CueR activates homeostasis gene expression at elevated copper concentrations, while CopY and CsoR repress their target genes under copper-limiting conditions. Besides these one-component systems, which sense the cytoplasmic copper status, many Gram-negative bacteria utilize two-component systems, which sense periplasmic copper concentrations. In addition to these well-studied transcriptional factors, copper control mechanisms acting at the post-transcriptional and the post-translational levels will be discussed.201222918892