Arabidopsis thaliana
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ABSTRACT:
PROVIDER: PRJNA324850 | ENA |
REPOSITORIES: ENA
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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:Differential regulation of HSFA1s and HSFA2 after heat shock in Arabidopsis
| PRJNA190712 | 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: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:FBXW7 modulates stress response by post-translational modification of HSF1 HSF1 orchestrates the heat-shock response upon exposure to heat stress and activates a transcriptional program vital for cancer cells. Genes positively regulated by HSF1 show increeased expression during heat shock while their expression is reduced during recovery. Genes negatively regulated by HSF1 show the opposite pattern. In this study we utilized the HCT116 FBXW7 KO colon cell line and its wild type counterpart to monitor gene expression changes during heat shock (42oC, 1 hour) and recovery (37oC for 2 hours post heat shock) using RNA sequencing. These results revealed that the heat-shock response pathway is prolonged in cells deficient for FBXW7. Whole RNA was extracted from 1 million HCT116 WT or FBXW7KO cells using the RNAeasy kit (Qiagen) according to the manufacturer’s protocol. Poly-A+ (magnetic oligodT-containing beads (Invitrogen)) or Ribominus RNA was used for library preparation. cDNA preparation and strand-specific library construction was performed using the dUTP method. Libraries were sequenced on the Illumina HiSeq 2000 using 50bp single-read method. Differential gene expression analysis was performed for each matched recovery versus heat-shock pairs, separately in each biological replicate and cell line (WT or KO). Two types of comparisons were tested: (a) WT recovery vs WT heat shock, (b) FBXW7 KO recovery vs heat shock.
2015-02-20 | E-GEOD-57397 | biostudies-arrayexpress
Project description:FBXW7 modulates stress response by post-translational modification of HSF1 HSF1 orchestrates the heat-shock response upon exposure to heat stress and activates a transcriptional program vital for cancer cells. Genes positively regulated by HSF1 show increeased expression during heat shock while their expression is reduced during recovery. Genes negatively regulated by HSF1 show the opposite pattern. In this study we utilized the HCT116 FBXW7 KO colon cell line and its wild type counterpart to monitor gene expression changes during heat shock (42oC, 1 hour) and recovery (37oC for 2 hours post heat shock) using RNA sequencing. These results revealed that the heat-shock response pathway is prolonged in cells deficient for FBXW7.
2015-02-20 | GSE57397 | GEO