Arabidopsis thaliana
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ABSTRACT:
PROVIDER: PRJNA95573 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:HSFA1s are a gene family of HSFA1 with four members, HSFA1a, HSFA1b, HSFA1d, and HSFA1e. HSFA1s are the master regulators of heat shock response. As a part of the heat shock response, HSFA2 can prolong the heat shock response and amplify the heat shock response in response to repeat heat shock. To identify the heat-shock-responsive genes differentially regulated by HSFA1s and HSFA2, we compared the transcriptomic differences of plants containing only constitutively expressed HSFA1s or HSFA2 after heat stress.
2013-04-09 | GSE44655 | GEO
Project description:HSFA1s are a gene family of HSFA1 with four members, HSFA1a, HSFA1b, HSFA1d, and HSFA1e. HSFA1s are the master regulators of heat shock response. As a part of the heat shock response, HSFA2 can prolong the heat shock response and amplify the heat shock response in response to repeat heat shock. To identify the heat-shock-responsive genes differentially regulated by HSFA1s and HSFA2, we compared the transcriptomic differences of plants containing only constitutively expressed HSFA1s or HSFA2 after heat stress. hsfa2 (the KO mutant of HSFA2, Col-0 background) and A2QK-10 (CaMV 35S:HSFA2 in QK mutant; QK is HSFA1a/b/d/e quadruple KO mutant) were used to compare the difference of heat shock response when plants lack HSFA1s or HSFA2. The aim is to find the HSFA1s- and HSFA2-preferred regulating genes after heat stress. As the control samples, wild type is the plant with normal heat shock response, and QK (HSFA1s KO mutant, Col-0 and Ws mixed background) is the plant that lost the heat shock response controlled by HSFA1s.
2013-04-09 | E-GEOD-44655 | biostudies-arrayexpress
Project description:We investigated the root growth of several knockout mutants of heat shock protein family genes and found that heat stress response was compromised in these mutants compared to wild type plants. It suggested that heat shock protein genes including heat shock protein genes including HSP17s, HSP23s, HSP101, and HSFA2 proteins are deployed upon exposure to Cs for plant stress tolerance. Our study provided novel insights into the molecular events occurring in Cs-stressed plants.
2024-04-06 | GSE262902 | 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 til1-1 mutant plants
| PRJNA113083 | ENA
Project description:Heat shock response in Arabidopsis Hsa32 knockout mutant
| PRJNA95209 | 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:Differential regulation of HSFA1s and HSFA2 after heat shock in Arabidopsis
| PRJNA190712 | ENA
Project description:Plants regulate growth and development in different ambient environments through light signaling pathways and heat stress signaling pathways, both of which are very important for plant adaptation to the environment, but whether there is an interaction between the two is still unclear. In this article, we reported that the blue light receptor Cryptochrome CRY1 phosphorylation will be inhibited under high temperature stress, and CRY1 activity will decrease; at this time, CRY1 could not interact with E3 ubiquitin ligase COP1(CONSTITUTIVELY PHOTOMORPHOGENIC 1) and COP1 activity increased. Its substrate HY5(ELONGATED HYPOCOTYL 5）is continuously degraded under heat stress. Through further transcriptome analysis, we found that the substrates of HY5 have a class of HSFAs（HEAT SHOCK FACTOR）HSFA2/HSFA7As/HSFA7Bs transcription factors, which are rapidly induced under heat stress conditions and activate downstream HSPs (HEAT SHOCK PROTEIN)expression.Under normal conditions, HY5 protein inhibits HSFA2/HSFA7As/HSFA7Bs. Under heat stress, HY5 protein is degraded, which releases the expression of HSFAs, thereby enhancing plant heat tolerance. In this paper, we put forward the hypothesis that the phosphorylation of CRY1 seems to be a switch in the ambient environment , and through the regulation of phosphorylation level, the light and heat stress signal are transmitted downward, forming an light-heat signal interactive regulation pathway to regulate the growth and development of plants.
2024-02-06 | GSE254813 | GEO
Project description:Arabidopsis 5’-3’ exoribonuclease, AtXRN4, a homolog of yeast Xrn1p, functions in degradation of uncapped RNAs after de-capping step. While Xrn1p-dependent on plant XRN4’s targets for degradation is still limited. For understanding biological function of AtXRN4, we tested survivability of atxrn4 mutants under heat stress. Our results showed that atxrn4 mutants increased survival rate under short-term degradation is a main mRNA decay in yeast, knowledge heat stress compared with WT plants. Our microarray and mRNA decay assay showed that loss of AtXRN4 function caused reduction of mRNA degradation of heat shock factor A2 (HSFA2) and ethylene response factor 1 (ERF1). HSFA2 has been known as a key regulator in heat acclimation, was found as a target for AtXRN4 for degradation at non-stress condition. Heat stress applied on atxrn4-3 hsfa2 double mutant severely lacked heat tolerance phenotype of atxrn4 mutant. These results suggest that AtXRN4-mediated mRNA degradation linked to suppress heat acclimation.
2015-07-14 | GSE66369 | GEO