Genomic responses to arsenic in Synechocystis
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ABSTRACT:
ORGANISM(S): Synechocystis sp. PCC 6803
PROVIDER: GSE51383 | GEO | 2014/05/13
SECONDARY ACCESSION(S): PRJNA223267
REPOSITORIES: GEO
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Project description:Arsenic is an ubiquitous contaminant and a toxic metalloid which presents two main redox states in nature: arsenite [AsIII] and arsenate [AsV]. Arsenic resistance in Synechocystis sp. strain PCC 6803 is mediated by the arsBHC operon and two additional arsenate reductases encoded by the arsI1 and arsI2 genes. Here we describe the genome-wide responses in response to the presence of arsenate and arsenite in wild type and in mutants in the arsenic resistance system. Both forms of arsenic produced similar responses in the wild type strain including induction of several stress related genes and repression of energy generation processes. The responses observed in the arsB mutant strain were similar to the wild type in short term but were maintained in time while they were only transient in the wild type strain. In contrast, the responses observed in a strain lacking all arsenate reductases (the SARS12 strain) were somewhat different and included lower induction of genes involved in metal homeostasis and Fe-S cluster biogenesis. These results suggest that these two processes are targeted by arsenite in the wild type strain. Finally, analysis of the arsR mutant strain revealed that ArsR seems to only control 5 genes in the genome. Furthermore, over-expression of ArsB conferred hypersentivity to nickel, copper and cadmium in an arsR mutant strain. Analysis of genome-wide gene expression patterns in response to arsenic in WT and mutants involved in arsenic detoxification in the cyanobacterium Synechocystis sp PCC 6803. Cells treated with arsenate or arsenite for 1h. Details: WT cells were treated with 1 mM arsenite for 1 h and its expression profile compared to untreated cells (grown in BG11C media). The effects of arsenate were analyzed in the same way but using a modified BG11C media that constains 15% of the normal phosphate concentration (BG11C low phosphate). A reduction in the phosphate concentration in the media is essential to detect grow inhibition after arsenate addition. In the same way that for arsenite cells were treated with 50 mM arsenate for 1 h and their expression profile was compared to untreated cells. Expression profiles of mutant strains lacking arsB gene (SARSB strain; this strain is hypersensitive to arsenite because it lacks the arsenite exporter) or arsR gene (SARSR strain; this strain expresses the arsBHC constitutively) in control conditions and in response to arsenite addition were also analyzed. In addition the expression profiles of a mutant lacking arsenate reductases (SARS12 strain that has interrupted arsC, arsI1 and arsI2 genes; this strain is hypersensitive to arsenate) were analyzed in both control conditions and after addition of 50 mM arsenate.
2014-05-13 | E-GEOD-51383 | biostudies-arrayexpress
Project description:ABSTRACT: Inorganic arsenic is a carcinogen and its ingestion in foods such as rice presents a significant risk to human health. Plants chemically reduce arsenate to arsenite. Using genome-wide association (GWA) mapping of loci controlling natural variation in arsenic accumulation in Arabidopsis thaliana allowed us to identify the arsenate reductase required for this reduction, which we named High Arsenic Content1 (HAC1). Complementation verified the identity of HAC1, and expression in Escherichia coli lacking a functional arsenate reductase confirmed the arsenate reductase activity of HAC1. The HAC1 protein accumulates in the epidermis, the outer cell layer of the root, and also in the pericycle cells surrounding the central vascular tissue. Plants lacking HAC1 lose their ability to efflux arsenite from roots, leading to both increased transport of arsenic into the central vascular tissue and on into the shoot. HAC1 therefore functions to reduce arsenate to arsenite in the outer cell layer of the root, facilitating efflux of arsenic as arsenite back into the soil to limit its accumulation in the root and transport to the shoot. Arsenate reduction by HAC1 in the pericycle may play a role in limiting arsenic loading into the xylem. Loss of HAC1 encoded arsenic reduction leads to a significant increase in arsenic accumulation in shoots causing an increased sensitivity to arsenate toxicity. We also confirmed the previous observation that the ACR2 arsenate reductase in A. thaliana plays no detectable role in arsenic metabolism. Further, ACR2 does not interact epistatically with HAC1, since arsenic metabolism in the acr2 hac1 double mutant is disrupted in an identical manner to that described for the hac1 single mutant. Our identification of HAC1 and its associated natural variation provides an important new resource for the development of low arsenic containing food stuffs such as rice.
2014-10-15 | GSE62299 | GEO
Project description:ABSTRACT: Inorganic arsenic is a carcinogen and its ingestion in foods such as rice presents a significant risk to human health. Plants chemically reduce arsenate to arsenite. Using genome-wide association (GWA) mapping of loci controlling natural variation in arsenic accumulation in Arabidopsis thaliana allowed us to identify the arsenate reductase required for this reduction, which we named High Arsenic Content1 (HAC1). Complementation verified the identity of HAC1, and expression in Escherichia coli lacking a functional arsenate reductase confirmed the arsenate reductase activity of HAC1. The HAC1 protein accumulates in the epidermis, the outer cell layer of the root, and also in the pericycle cells surrounding the central vascular tissue. Plants lacking HAC1 lose their ability to efflux arsenite from roots, leading to both increased transport of arsenic into the central vascular tissue and on into the shoot. HAC1 therefore functions to reduce arsenate to arsenite in the outer cell layer of the root, facilitating efflux of arsenic as arsenite back into the soil to limit its accumulation in the root and transport to the shoot. Arsenate reduction by HAC1 in the pericycle may play a role in limiting arsenic loading into the xylem. Loss of HAC1 encoded arsenic reduction leads to a significant increase in arsenic accumulation in shoots causing an increased sensitivity to arsenate toxicity. We also confirmed the previous observation that the ACR2 arsenate reductase in A. thaliana plays no detectable role in arsenic metabolism. Further, ACR2 does not interact epistatically with HAC1, since arsenic metabolism in the acr2 hac1 double mutant is disrupted in an identical manner to that described for the hac1 single mutant. Our identification of HAC1 and its associated natural variation provides an important new resource for the development of low arsenic containing food stuffs such as rice. Hybridizations from a set of Bulk Segregant analysis. We measured the elemental profile of 315 F2 plants from a cross between the high arsenic Arabidopsis thaliana accession Kr-0 and the the low arsenic accession Col-0, data available at www.ionomicshub.org <http://www.ionomicshub.org>. Leaves from the 59 highest and 61 lowest arsenic accumulating plants (calculated as a percentage of the Col-0 accumulation in the same growth tray) were pooled and the genomic DNA was extracted using Qiagen kits.
2014-10-15 | E-GEOD-62299 | biostudies-arrayexpress
Project description:Arsenic (As) 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 host in arsenic-rich conditions can provide novel insights into dynamics of host-microbe-microenvironment 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 (Xoo), which is a serious plant pathogen infecting rice. Our study revealed the horizontal acquisition of a novel chromosomal 12kb ars cassette in Xoo 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. This cassette has spread in lineage with highly virulent strains owing to a particular lineage’s evolutionary success. Further, we performed the transcriptomic analysis of Xoo strain IXO1088 under arsenate/arsenite exposure using RNA sequencing. The transcriptomic analysis revealed that arsenic detoxification and efflux, oxidative stress response, iron acquisition/storage, and damage repair are the main cellular responses to arsenic exposure. The study provides useful insights into the acquisition, detoxification, and adaptation mechanisms among Xoo populations to adapt under arsenic-rich environmental conditions.
2021-05-17 | GSE163417 | GEO
Project description:To analyse the transcriptional response of Rhodococcus aetherivornas BCP1 to arsenic, RNA was extracted from BCP1 cultures exposed to arsenite [As(III)] 5 mM and arsenate [As(V)] 30 mM for 18 hours in the presence of glucose as only carbon and energy source. Control cultures were carried out without adding any arsenic oxyanions. Illumina Truseq stranded mRNA libraries were constructed after rRNA depletion via Illumina Ribozero and sequenced on Illumina HiSeq 1500 system 2 x 70nt PE rapid mode.
2021-12-31 | E-MTAB-10692 | biostudies-arrayexpress
Project description:To identified the differential expressed genes between the arsenic exposure cells and wild type cells As is a well- known carcinogen, it receives special attention. Due to its ubiquitous distribution in the environment, a unicellular model system related to the environment will be useful in toxicological research of arsenic. The eukaryotic protist Tetrahymena thermophila is a well-established model in classical toxicology and now a potential model at genomic level. In the present study, Tetrahymena thermophila was inbred with arsenate. With the use of microarray technique, the genes differentially expressed at 4 time points in exposure to arsenate were screened out. The major biological processes involved and their changes over time were identified with enrichment analysis and transformed expression data. Characteristics of arsenic toxicity and response to arsenic were identified, proving T. thermophila a good unicellular model for arsenic toxicological research at genomic level.
2019-12-01 | GSE53836 | GEO
Project description:Arsenic (As) exposure is a significant worldwide environmental health concern. Low dose, chronic arsenic exposure has been associated with higher risk of skin, lung, and bladder cancer, as well as cardiovascular disease and diabetes. While arsenic-induced biological changes play a role in disease pathology, little is known about the dynamic cellular changes due to arsenic exposure and withdrawal. In these studies, we seek to understand the molecular mechanisms behind the biological changes induced by chronic low doses of arsenic exposure. We used a comprehensive approach involving chromatin structural studies and mRNA microarray analyses to determine how chromatin structure and gene expression patterns change in response to chronic low dose arsenic exposure and its subsequent withdrawal. Our results show that cells exposed to low doses of sodium arsenite have distinct temporal and coordinated chromatin, gene expression and miRNA changes that are consistent with differentiation and activation of multiple biochemical pathways. Most of these temporal patterns in gene expression are reversed when arsenic was withdrawn. However, some of the gene expression patterns remained altered, plausibly as a result of an adaptive response by these cells. Additionally, these gene expression patterns correlated with changes in chromatin structure, further solidifying the role of chromatin structure in gene regulatory changes due to arsenite exposure. Lastly, we show that arsenite exposure influences gene regulation both at the transcription initiation as well as at the splicing level. Thus our results suggest that general patterns of alternative splicing, as well as expression of particular gene regulators, can be indicative of arsenite-induced cell transformation. A total of eight (8) samples with two biological replicates under four separate conditions: wild-type treated with deionized H2O for 36 days (NT); chronic low-dose arsenic exposure of 1 uM of sodium arsenite (iAs-T) for 36 days; chronic arsenic exposure of 1 uM of sodium arsenite for 26 days followed by removal of sodium arsenite for 10 days, measured at day 36 (iAs-Rev); and chronic arsenic exposure of 1 uM of sodium arsenite for 26 days, followed by removal of sodium arsenite exposure for 10 days, followed by 1 uM of chronic sodium arsenite exposure for 10 days (measured at day 46) (iAs-Rev-T).
2015-05-05 | E-GEOD-60760 | biostudies-arrayexpress
Project description:Arsenic is known as a human carcinogen that easily be exposed by the living organisms through environment and food consumption. The arsenic is transport into the cells via phosphate transporters due to its structural similarity with phosphate in both prokaryotes and eukaryotes. We here evaluated and analyzed the toxicogenomic impacts of arsenate and the role of different phosphate concentrations on arsenic toxicity. Our results showed that arsenic uncoupled phosphate levels which eventually affected the growth rate of yeast cells. Analysis of arsenate levels in the medium over 4 to 10 h of its exposure clearly showed that arsenate was easily taken up by the cells in phosphate limited condition.
2009-12-31 | GSE14991 | GEO
Project description:Arsenic metalloid is a double-edge sword. On the one hand it is a very toxic and powerful carcinogen, and on the other it has been successfully used in the treatment of acute promyelocytic leukemia. In order to prevent the deleterious effects caused by arsenic compounds, almost all living organisms have developed mechanisms to eliminate it. In this study genome-wide response of S. cerevisiae to arsenic shows that this metal interferes with genes involved in the iron homeostasis including those encoding proteins that function in iron uptake, incorporation into Fe–S clusters, and more. In addition our data indicate that Yap1 transcriptionally controls the iron homeostasis regulator AFT2 as well as its direct target, MRS4. Most importantly in response to arsenate exposure Yap1 strongly regulates the expression of several genes involved in the Fe-S proteins biosynthesis, namely NBP35 and YFH1. Interestingly mRNA levels encoding Fet3, Ferro-O2-oxidoreductase required for high-affinity iron uptake, are drastically destabilized upon arsenic exposure. Such destabilization is due to the 5’ to 3’ exonuclease Xrn1 localized in the P Bodies. Moreover FET3 mRNA decay is not mediated by Cth2 and is independent on the formation of ROS responsible for the toxic effects of arsenic compounds. Strikingly, in presence of arsenate fet3 mutant shows resistance over the wild-type which leads us to suggest that Fet3 has a role in arsenic toxicity. Unexpectedly arsenic treatment seems to activate the non-reductive iron uptake in order to maintain the cellular iron homeostasis. Furthermore our genetic, biochemical, and physiological analysis demonstrate that aft1 mutant is sensitive to arsenic compounds and such phenotype is reversible upon addition of iron. We also show that arsenic exposure induces iron deficiency in aft1 mutant. In conclusion this work shows for the first time that arsenic, a chemotherapy drug used to treat a specific type of acute promyelocytic leukemia (APL), disrupts iron homeostasis and our results suggest that this disruption is independent on ROS generation. Finally we provide preliminary data confirming that such disruption also takes place in mammalian cells, an observation that can be very relevant in term of clinical applications.
2011-11-04 | GSE33427 | GEO
Project description:Stress constantly challenges plant adaptation to the environment. Of all stress types, arsenic was a major threat during the early evolution of plants. The most prevalent chemical form of arsenic is arsenate, whose similarity to phosphate renders it easily incorporated into cells via the phosphate transporters. Here we found that arsenate stress provokes a notable transposon burst in plants, in coordination with arsenate/phosphate transporter repression, which immediately restricts arsenate uptake. This repression was accompanied by delocalization of the phosphate transporter from the plasma membrane. When arsenate was removed, the system rapidly restored transcriptional expression and membrane localization of the transporter. We identify WRKY6 as an arsenate-responsive transcription factor that mediates arsenate/phosphate transporter gene expression and restricts arsenate-induced transposon activation. Plants therefore have a dual WRKY-dependent signaling mechanism that modulates arsenate uptake and transposon expression, providing a coordinated strategy for arsenate tolerance and transposon gene silencing.
2014-04-25 | GSE49037 | GEO