E-GEOD-5539
Ontology highlight
ABSTRACT:
PROVIDER: E-GEOD-5539 | ExpressionAtlas | 2014-07-03
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-5539-analysis-methods.tsv | Tabular | |||
| E-GEOD-5539-atlasExperimentSummary.Rdata | Rdata | |||
| E-GEOD-5539-configuration.xml | Xml | |||
| E-GEOD-5539-percentile-ranks.tsv | Tabular | |||
| E-GEOD-5539-zoomifications-log.tsv | Tabular |
Items per page: 5 1 - 5 of 65 |
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Project description:Over-expression of MBF1c enhances stress tolerance
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Project description:Multiprotein bridging factor 1c MBF1c (At3g24500) is a stress-response transcription co-activator. To test the function of MBF1c, we over-expressed it in transgenic Arabidopsis plants using the 35S-CaMV promoter. T4 seeds form 3 independent lines were tested for their tolerance to biotic and abiotic stress conditions. Constitutive expression of MBF1c in Arabidopsis enhanced the tolerance of transgenic plants to bacterial infection, salinity, heat and osmotic stress. Moreover, the enhanced tolerance of transgenic plants to osmotic and heat stress was maintained even when these two stresses were combined. The expression of MBF1c in transgenic plants augmented the accumulation of a number of sugars and defense transcrtipts in response to heat stress. Transcriptome profiling and inhibitor studies suggest that MBF1c expression enhances the tolerance of transgenic plants to heat and osmotic stress by partially activating, or perturbing, the ethylene-response signal transduction pathway. MBF1 proteins could be used to enhance the tolerance of plants to different abiotic stresses. Suzuki et al., 2005 Plant Physiology, submitted. Experimenter name = Ron Mittler; Experimenter phone = 1-775-784-1384; Experimenter fax = 1-775-784-1650; Experimenter department = Dept. of Biochemistry; Experimenter institute = University of Nevada; Experimenter address = MS200; Experimenter address = Reno; Experimenter address = Nevada; Experimenter zip/postal_code = 89557; Experimenter country = USA Experiment Overall Design: 6 samples were used in this experiment
2008-06-13 | E-GEOD-5539 | biostudies-arrayexpress
Project description:Multiprotein bridging factor 1c MBF1c (At3g24500) is a stress-response transcription co-activator. To test the function of MBF1c, we over-expressed it in transgenic Arabidopsis plants using the 35S-CaMV promoter. T4 seeds form 3 independent lines were tested for their tolerance to biotic and abiotic stress conditions. Constitutive expression of MBF1c in Arabidopsis enhanced the tolerance of transgenic plants to bacterial infection, salinity, heat and osmotic stress. Moreover, the enhanced tolerance of transgenic plants to osmotic and heat stress was maintained even when these two stresses were combined. The expression of MBF1c in transgenic plants augmented the accumulation of a number of sugars and defense transcrtipts in response to heat stress. Transcriptome profiling and inhibitor studies suggest that MBF1c expression enhances the tolerance of transgenic plants to heat and osmotic stress by partially activating, or perturbing, the ethylene-response signal transduction pathway. MBF1 proteins could be used to enhance the tolerance of plants to different abiotic stresses. Suzuki et al., 2005 Plant Physiology, submitted. Experimenter name = Ron Mittler Experimenter phone = 1-775-784-1384 Experimenter fax = 1-775-784-1650 Experimenter department = Dept. of Biochemistry Experimenter institute = University of Nevada Experimenter address = MS200 Experimenter address = Reno Experimenter address = Nevada Experimenter zip/postal_code = 89557 Experimenter country = USA Keywords: genetic_modification_design; stimulus_or_stress_design
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Project description:Plants adapt to cold, non-freezing temperatures through cold acclimation and subsequently lose the acquired freezing tolerance in warmer temperatures in a process called deacclimation. By measuring the freezing tolerance of mutant lines, this study identified that the loss of HRA1, LBD41, MBF1c and JUB1 slows the rate of deacclimation in the first four days in Arabidopsis thaliana. Comparative transcriptomic (RNA-Seq) and co-expression analysis of Col-0, mbf1c and jub1 during deacclimation identified an involvement of thermoswitches, cell wall remodeler and transporters in the regulation of the rate of deacclimation. In mbf1c and jub1 a unique increase in stress responsive genes and regulation of the jasmonic acid pathway was detected and linked to the mutants’ retention of freezing tolerance during deacclimation. Hypoxia was observed to be induced in early deacclimation evidenced by an increase in ADH enzyme activity and upregulated gene expression of hypoxia markers (qRT-PCR). This work suggests that the overserved hypoxia response creates hypoxic niches within the plants and supports growth and development during deacclimation.
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Project description:Abiotic stresses cause serious damage to plants; therefore, plants undergo a complicated stress response through signal transduction originating from environmental stimuli. Here we show that a subset of short-chain leaf volatiles with an α,β-unsaturated carbonyl bond in their structure (reactive short-chain leaf volatiles, RSLVs) like (E)-2-hexenal and (E)-2-butenal can act as signal chemicals that strongly induce the gene expression of abiotic-related transcription factors, such as heat stress-related transcription factors (HSFA2, MBF1c) and other abiotic stress-related transcription factors (DREB2A, ZATs). RSLV-induced expression of HSFA2 and MBF1c was eliminated in HSFA1s-, known as heat stress response master regulators, knockout mutant, whereas those of DREB2A and ZATs were not, suggesting that the RSLV signaling pathway is composed of HSFA1-dependent and -independent pathways. RSLV treatment induced production of chaperon proteins, and the RSLV-treated Arabidopsis thus demonstrated enhanced abiotic stress tolerance. Because oxidative stress treatment enhanced RSLV production, we concluded that commonly found RSLVs produced by environmental stresses are powerful inducer of abiotic stress-related gene expression as oxidative stress signals.
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Project description:Abiotic stresses cause serious damage to plants; therefore, plants undergo a complicated stress response through signal transduction originating from environmental stimuli. Here we show that a subset of short-chain leaf volatiles with an α,β-unsaturated carbonyl bond in their structure (reactive short-chain leaf volatiles, RSLVs) like (E)-2-hexenal and (E)-2-butenal can act as signal chemicals that strongly induce the gene expression of abiotic-related transcription factors, such as heat stress-related transcription factors (HSFA2, MBF1c) and other abiotic stress-related transcription factors (DREB2A, ZATs). RSLV-induced expression of HSFA2 and MBF1c was eliminated in HSFA1s-, known as heat stress response master regulators, knockout mutant, whereas those of DREB2A and ZATs were not, suggesting that the RSLV signaling pathway is composed of HSFA1-dependent and -independent pathways. RSLV treatment induced production of chaperon proteins, and the RSLV-treated Arabidopsis thus demonstrated enhanced abiotic stress tolerance. Because oxidative stress treatment enhanced RSLV production, we concluded that commonly found RSLVs produced by environmental stresses are powerful inducer of abiotic stress-related gene expression as oxidative stress signals.
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Project description:Abiotic stresses cause serious damage to plants; therefore, plants undergo a complicated stress response through signal transduction originating from environmental stimuli. Here we show that a subset of short-chain leaf volatiles with an M-NM-1,M-NM-2-unsaturated carbonyl bond in their structure (reactive short-chain leaf volatiles, RSLVs) like (E)-2-hexenal and (E)-2-butenal can act as signal chemicals that strongly induce the gene expression of abiotic-related transcription factors, such as heat stress-related transcription factors (HSFA2, MBF1c) and other abiotic stress-related transcription factors (DREB2A, ZATs). RSLV-induced expression of HSFA2 and MBF1c was eliminated in HSFA1s-, known as heat stress response master regulators, knockout mutant, whereas those of DREB2A and ZATs were not, suggesting that the RSLV signaling pathway is composed of HSFA1-dependent and -independent pathways. RSLV treatment induced production of chaperon proteins, and the RSLV-treated Arabidopsis thus demonstrated enhanced abiotic stress tolerance. Because oxidative stress treatment enhanced RSLV production, we concluded that commonly found RSLVs produced by environmental stresses are powerful inducer of abiotic stress-related gene expression as oxidative stress signals. A four chips study of Columbia-0 following 10 M-BM-5M 2E-hexenal treatment for 30 min. Datasets including acetonitrile (control) and 2E-hexenal treated samples (triplicates).
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Project description:Abiotic stresses cause serious damage to plants; therefore, plants undergo a complicated stress response through signal transduction originating from environmental stimuli. Here we show that a subset of short-chain leaf volatiles with an M-NM-1,M-NM-2-unsaturated carbonyl bond in their structure (reactive short-chain leaf volatiles, RSLVs) like (E)-2-hexenal and (E)-2-butenal can act as signal chemicals that strongly induce the gene expression of abiotic-related transcription factors, such as heat stress-related transcription factors (HSFA2, MBF1c) and other abiotic stress-related transcription factors (DREB2A, ZATs). RSLV-induced expression of HSFA2 and MBF1c was eliminated in HSFA1s-, known as heat stress response master regulators, knockout mutant, whereas those of DREB2A and ZATs were not, suggesting that the RSLV signaling pathway is composed of HSFA1-dependent and -independent pathways. RSLV treatment induced production of chaperon proteins, and the RSLV-treated Arabidopsis thus demonstrated enhanced abiotic stress tolerance. Because oxidative stress treatment enhanced RSLV production, we concluded that commonly found RSLVs produced by environmental stresses are powerful inducer of abiotic stress-related gene expression as oxidative stress signals. A four chips study of Columbia-0 following 10 M-BM-5M 2E-pentenal, 3-hepten-2-one or crotonaldehydel treatment for 30 min. Datasets including acetonitrile (control) and volatiles treated samples.
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