GLABRA2 Transcription Factor integrates Arsenic tolerance with cell differentiation in Epidermal Cells [Exp1]
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ABSTRACT:
PROVIDER: PRJNA1073455 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR27872800.fastq.gz | Fastqsanger.gz | |||
| SRR27872789.fastq.gz | Fastqsanger.gz | |||
| SRR27872790.fastq.gz | Fastqsanger.gz | |||
| SRR27872791.fastq.gz | Fastqsanger.gz | |||
| SRR27872792.fastq.gz | Fastqsanger.gz |
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Project description:Arsenic poses a global threat to living organisms, compromising crop security and yield. Limited understanding of the transcriptional network integrating arsenic tolerance mechanisms with plant developmental responses hinders the development of strategies against this menace. Here, we employed an integrative genomic approach in Arabidopsis thaliana, involving a high-throughput yeast one-hybrid assay, and a transcriptomic analysis coupled with a transcription factor binding site enrichment analysis in gene expression clusters, to uncover novel transcriptional regulators of the arsenic response. We identified the GLABRA2 (GL2) transcription factor as a novel regulator of arsenic tolerance, revealing a wider regulatory role beyond its established function as a repressor of root hair formation. Furthermore, we found that ANTHOCYANINLESS2 (ANL2), a GL2 subfamily member, acts redundantly with this transcription factor in the regulation of arsenic signaling. Both transcription factors act as repressors of arsenic response. gl2 and anl2 mutants exhibit enhanced tolerance and reduced arsenic accumulation. Transcriptional analysis in the gl2 mutant unveils potential regulators of arsenic tolerance. These findings highlight GL2 and ANL2 as novel integrators of the arsenic response with developmental outcomes, offering insights for developing safer crops with reduced arsenic content and increased tolerance to this hazardous metalloid.
2024-08-31 | GSE255065 | GEO
Project description:GLABRA2 Transcription Factor integrates Arsenic tolerance with cell differentiation in Epidermal Cells
| PRJNA1073449 | ENA
Project description:GLABRA2 Transcription Factor integrates Arsenic tolerance with cell differentiation in Epidermal Cells [Exp2]
| PRJNA1073469 | ENA
Project description:Arsenic poses a global threat to living organisms, compromising crop security and yield. Limited understanding of the transcriptional network integrating arsenic tolerance mechanisms with plant developmental responses hinders the development of strategies against this menace. Here, we employed an integrative genomic approach in Arabidopsis thaliana, involving a high-throughput yeast one-hybrid assay, and a transcriptomic analysis coupled with a transcription factor binding site enrichment analysis in gene expression clusters, to uncover novel transcriptional regulators of the arsenic response. We identified the GLABRA2 (GL2) transcription factor as a novel regulator of arsenic tolerance, revealing a wider regulatory role beyond its established function as a repressor of root hair formation. Furthermore, we found that ANTHOCYANINLESS2 (ANL2), a GL2 subfamily member, acts redundantly with this transcription factor in the regulation of arsenic signaling. Both transcription factors act as repressors of arsenic response. gl2 and anl2 mutants exhibit enhanced tolerance and reduced arsenic accumulation. Transcriptional analysis in the gl2 mutant unveils potential regulators of arsenic tolerance. These findings highlight GL2 and ANL2 as novel integrators of the arsenic response with developmental outcomes, offering insights for developing safer crops with reduced arsenic content and increased tolerance to this hazardous metalloid.
2024-08-31 | GSE255066 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2024-08-31 | GSE255067 | GEO
Project description:Transcriptional profiling of arsenic-induced toxicity and tolerance in Arabidopsis plants of different ecotypes Arsenic (As) is a toxic metalloid found ubiquitously in the environment and has widely been known as an acute poison and carcinogen. As toxicity is a major factor leading to root growth inhibition in plants. However, the molecular mechanisms of plants in response to As has not been extensively characterized. In this study, Arabidopsis ecotypes that are As-tolerant (Col-0) and -sensitive (Ws-2) were used to conduct a transcriptome analysis of the response to As (V). To begin elucidating the molecular basis of As toxicity and tolerance in Arabidopsis, seedlings of Col-0 and Ws-2 were subjected to As treatment. The root elongation rate of Col-0 was significantly higher than that of Ws-2 when exposed to As. The tolerant ecotype (Col-0) demonstrated lower accumulation of As when compared to the responses observed in the sensitive Ws-2. Subsequently, the effect of As exposure on genome-wide gene expression was examined in the two ecotypes. Comparative analysis of microarray data identified groups of genes with common and specific responses to As between Col-0 and Ws-2. The genes related to heat responses and oxidative stresses belonged to common responses, indicating conserved stress-associated changes across two ecotypes. The majority of specific responsive genes were those encoding heat shock proteins, heat shock factors, ubiquitin and transporters. The data suggested that metal transport and maintenance of protein structure may be important mechanisms for toxicity and tolerance to As. This study presents comprehensive surveys of global transcriptional regulation and identifies stress- and tolerance-associated genes in response to As. Comparison of Arabidopsis ecotype Col-0 and Ws-2 in response to As with the Affymetrix GeneChip were performed by the Affymetrix Gene Expression Service Lab (http://ipmb.sinica.edu.tw/affy/), supported by Academia Sinica, Taiwan
2011-11-26 | E-GEOD-31977 | biostudies-arrayexpress
Project description:The purpose of this study is to search for aberrant genes in HaCaT keratinocytes after chronic exposure to arsenic trioxide. The objective of the investigation was to discover the mechanism of arsenic carcinogenicity in human epidermal keratinocytes. We hypothesize that a combined strategy of DNA microarray, qRT-PCR and gene function annotation will identify aberrantly expressed genes in HaCaT keratinocyte cell line after chronic treatment with arsenic trioxide. HaCaT cells were chronically exposed to 0.5µg/mL arsenic trioxide (As2O3) up to 22 passages and RNA was extracted. Microarray data analysis identified 14 up-regulated genes and 21 down-regulated genes in response to arsenic trioxide
2012-04-12 | GSE37192 | GEO
Project description:Transcriptional profiling of arsenic-induced toxicity and tolerance in Arabidopsis plants of different ecotypes Arsenic (As) is a toxic metalloid found ubiquitously in the environment and has widely been known as an acute poison and carcinogen. As toxicity is a major factor leading to root growth inhibition in plants. However, the molecular mechanisms of plants in response to As has not been extensively characterized. In this study, Arabidopsis ecotypes that are As-tolerant (Col-0) and -sensitive (Ws-2) were used to conduct a transcriptome analysis of the response to As (V). To begin elucidating the molecular basis of As toxicity and tolerance in Arabidopsis, seedlings of Col-0 and Ws-2 were subjected to As treatment. The root elongation rate of Col-0 was significantly higher than that of Ws-2 when exposed to As. The tolerant ecotype (Col-0) demonstrated lower accumulation of As when compared to the responses observed in the sensitive Ws-2. Subsequently, the effect of As exposure on genome-wide gene expression was examined in the two ecotypes. Comparative analysis of microarray data identified groups of genes with common and specific responses to As between Col-0 and Ws-2. The genes related to heat responses and oxidative stresses belonged to common responses, indicating conserved stress-associated changes across two ecotypes. The majority of specific responsive genes were those encoding heat shock proteins, heat shock factors, ubiquitin and transporters. The data suggested that metal transport and maintenance of protein structure may be important mechanisms for toxicity and tolerance to As. This study presents comprehensive surveys of global transcriptional regulation and identifies stress- and tolerance-associated genes in response to As.
2011-11-26 | GSE31977 | GEO
Project description:Purpose: To determine the effects of sodium arsenite in male mice on adaptive thermogenesis. Methods: Male C57BL/6J mice were exposed to sodium arsenite in drinking water at 300 parts per billion (ppb) for 9 weeks Findings: Arsenic-treated mice experienced significantly decreased metabolic heat production when acclimated to chronic cold tolerance testing, as evidenced by indirect calorimetry, despite no change in physical activity. Arsenic exposure increased total fat mass, and unilocular lipid droplet size in both subcutaneous inguinal white adipose tissue (iWAT) and brown adipose tissue (BAT). Conclusion: Chronic arsenic exposure impacts the mitochondria of thermogenic tissues involved in energy expenditure and glucose regulation, providing novel mechanistic evidence for arsenic’s role in metabolic pathologies.
2020-01-01 | GSE134982 | GEO