Arabidopsis thaliana
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ABSTRACT:
PROVIDER: PRJNA324850 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:In this study we perform precision nuclear run-on sequencing (PRO-seq) to measure the altered transcriptional response upon CDK7 inhibition or RNA-seq to elucidate the response of CDK7 inhibition on steady-state RNA. We performed a heat shock time course in PRO-seq with and without the Syros CDK7 inhibitor SY5609. Matching this data we performed three deeply sequenced RNA-seq experiments with SY5609 that include no heat shock, heat shock with recovery and long heat shock with no recovery. We additionally generated two more RNA-seq datasets in heat shock conditions with another Syros inhibitor, SY5102 and in a CDK7-analog sensitive OV90 cell line treated with 3MBPP1.
2024-12-19 | GSE228346 | GEO
Project description:The expression of heat-shock proteins (Hsps) induced by a non-lethal heat treatment confers acquired thermotolerance (AT) to organisms against a subsequent challenge of otherwise lethal temperature. After stress signal lifted, AT gradually decayed with the decline of Hsps during recovery period. The duration of AT may be critical for sessile organisms, such as plants, to survive repeated heat stress in the environment. To identify heat-induced genes involved in duration of AT, we took a reverse-genetics approach by screening for Arabidopsis T-DNA insertion mutants that show decreased thermotolerance after a long recovery at non-stress condition following a conditioning treatment. Among the tested mutants corresponding to 47 genes, only the HsfA2 knockout mutant showed significant phenotype. The mutant plants were more sensitive to severe heat stress than the wild type after long but not short recovery following a pretreatment at 37oC, which can be complemented by introducing a wild-type copy of the gene. Quantitative hypocotyl elongation assay also revealed that AT decayed faster in the absence of HsfA2. Significant decline of the transcript levels of several highly heat-induced genes was observed in the HsfA2 knockout plants after a 4-h recovery or after 2 h of prolonged heat stress. Immunoblot anlysis showed that Hsa32 and class I small Hsp were lower in the mutant than in the wild type after a long recovery. Our results suggest that HsfA2 as a heat-induced transactivator sustains the post-stress expression of Hsp genes and extends the duration of AT in Arabidopsis. Experiment Overall Design: Total RNA was isolated from the seedlings of 5-d old wild-type and HsfA2 knockout mutant seedlings (a pool of about 100 plants per treatment in duplicates) harvested immediately after heat shock treatment. In this experiment, total 12 chips were used, 1 each for 2 biological replicates of the control and HS-treated samples for the wild type and mutant plants.
2008-06-13 | E-GEOD-4760 | biostudies-arrayexpress
Project description:Heat shock response of HsfA2 knockout plants
| PRJNA95573 | ENA
Project description:Heat shock response of til1-1 mutant plants
| PRJNA113083 | ENA
Project description:Heat shock response in Arabidopsis Hsa32 knockout mutant
| PRJNA95209 | ENA
Project description:Plants and animals share similar mechanisms in the heat-shock (HS) response, such as synthesis of the conserved HS proteins (Hsps). However, because plants are confined to a growing environment, in general they require unique features to cope with heat stress. We have analyzed the function of a novel Hsp, heat-stress-associated 32-kD protein (Hsa32), which is highly conserved in land plants but absent in most other organisms. The gene responds to HS at the transcriptional level in moss, Arabidopsis, and rice. Like other Hsps, Hsa32 protein accumulates greatly in Arabidopsis seedlings after HS treatment. Disruption of Hsa32 by T-DNA insertion does not affect growth and development under normal conditions. However, the acquired thermotolerance in the knockout line was compromised following a long recovery period (> 24 h) after an acclimation HS treatment, when a severe HS challenge killed the mutant but not the wild-type plants, but no significant difference was observed if they were challenged within a short recovery period. Microarray analysis of the knockout mutant indicates that only the expression of Hsa32 was significantly altered in HS response. Taken together, our results suggest that Hsa32 is not required for the induction but maintenance of acquired thermotolerance. This report provides direct evidence that a plant-specific Hsp plays an important role in thermotolerance. Keywords: heat shock response
2006-03-20 | GSE4062 | GEO
Project description:Differential regulation of HSFA1s and HSFA2 after heat shock in Arabidopsis
| PRJNA190712 | ENA
Project description:Gene expression of Arabidopsis leaves under heat stress and during recovery
| PRJNA266755 | ENA
Project description:The expression of heat-shock proteins (Hsps) induced by a non-lethal heat treatment confers acquired thermotolerance (AT) to organisms against a subsequent challenge of otherwise lethal temperature. After stress signal lifted, AT gradually decayed with the decline of Hsps during recovery period. The duration of AT may be critical for sessile organisms, such as plants, to survive repeated heat stress in the environment. To identify heat-induced genes involved in duration of AT, we took a reverse-genetics approach by screening for Arabidopsis T-DNA insertion mutants that show decreased thermotolerance after a long recovery at non-stress condition following a conditioning treatment. Among the tested mutants corresponding to 47 genes, only the HsfA2 knockout mutant showed significant phenotype. The mutant plants were more sensitive to severe heat stress than the wild type after long but not short recovery following a pretreatment at 37oC, which can be complemented by introducing a wild-type copy of the gene. Quantitative hypocotyl elongation assay also revealed that AT decayed faster in the absence of HsfA2. Significant decline of the transcript levels of several highly heat-induced genes was observed in the HsfA2 knockout plants after a 4-h recovery or after 2 h of prolonged heat stress. Immunoblot anlysis showed that Hsa32 and class I small Hsp were lower in the mutant than in the wild type after a long recovery. Our results suggest that HsfA2 as a heat-induced transactivator sustains the post-stress expression of Hsp genes and extends the duration of AT in Arabidopsis. Keywords: heat shock response
2006-11-01 | GSE4760 | GEO
Project description:The heat shock response continues to be layered with additional complexity as interactions and cross-talk among heat shock proteins, the reactive oxygen network and hormonal signaling are discovered. However, comparative analyses exploring variation in each of these processes among species remains relatively unexplored. In controlled environment experiments, photosynthetic response curves were conducted from 22 °C to 42 °C and indicated that temperature optimum of light saturated photosynthesis was greater for Glycine max relative to Arabidopsis thaliana or Populus trichocarpa. Transcript profiles were taken at defined states along the temperature response curves and inferred pathway analysis revealed species-specific variation in the abiotic stress and the minor carbohydrate raffinose/galactinol pathways. A weighted gene co-expression network approach was used to group individual genes into network modules linking biochemical measures of the antioxidant system to leaf-level photosynthesis among P. trichocarpa, G. max and A. thaliana. Network enabled results revealed an expansion in the G. max HSP17 protein family and divergence in the regulation of the antioxidant and heat shock module relative to P. trichocarpa and A. thaliana. These results indicate that although the heat shock response is highly conserved, there is considerable species-specific variation in its regulation.
2011-04-01 | GSE26197 | GEO