Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1054519 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR27283646_1.fastq.gz | Fastqsanger.gz | |||
| SRR27283646_2.fastq.gz | Fastqsanger.gz | |||
| SRR27283647_1.fastq.gz | Fastqsanger.gz | |||
| SRR27283647_2.fastq.gz | Fastqsanger.gz | |||
| SRR27283648_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Plant cells are surrounded by walls, which must often meet opposing functional requirements during plant growth and defense. The cells meet them by modifying wall structure and composition in a tightly controlled and adaptive manner. The modifications seem to be mediated by a dedicated cell wall integrity (CWI) maintenance mechanism. Currently the mode of action of the mechanism is not understood and it is unclear how its activity is coordinated with established plant defense signaling. We investigated both the responses to cell wall damage (CWD) compromising CWI and the underlying mechanism in Arabidopsis thaliana. A cellulose biosynthesis inhibitor isoxaben was used as a tool to induce the loss of cell wall integrity. Isoxaben was chosen because it only affects a certain cell type / differentiation stage, and weakens the cell walls indirectly by inhibiting a biosynthetic process, making CWD occurrence dependent on high turgor levels (allowing simultaneous manipulation of the responses by addition of osmotica like sorbitol, mannitol, etc.). Isoxaben treatment causes structural damage, induction of lesion formation, cell death, deposition of lignin and callose as well as production of jasmonic acid and salicylic acid. Isoxaben-resistant mutant ixr1-1 is included to ensure the specificity of the treatment.
2018-01-11 | GSE108987 | GEO
Project description:The cell wall is a crucial structure in plant cells, and modifications in its composition often have a major impact on growth and development. However, the molecular mechanisms responsible for the negative effects of cell wall alterations on plant growth are largely unknown. It was previously shown that a reduction in the levels of de-esterified homogalacturonan, a major pectin component of cell walls, in Arabidopsis thaliana plants expressing a fungal polygalacturonase or mutated in the QUASIMODO2 gene (qua2-1 plants), cause severe growth defects. Here we show that the class III peroxidase AtPrx71 is strongly up-regulated in these plants, as well as in response to alterations of other wall structural components, including treatments the cellulose synthase inhibitor isoxaben. Analysis of atprx71 loss-of-function mutants and of plants overexpressing AtPrx71 indicates that this gene negatively affects Arabidopsis growth at different stages of development. Furthermore, lack of AtPrx71 partially suppresses the dwarf phenotype of qua2-1, suggesting that this protein contributes to the growth defects observed in plants undergoing cell wall damage. AtPrx71 appears to promote the production of reactive oxygen species in qua2-1 plants, as well as in plants treated with isoxaben. We propose that production of reactive oxygen species mediated by AtPrx71 negatively regulates Arabidopsis growth both during physiological development and in response to loss of cell wall integrity. Transcriptional profiling of Arabidopsis thaliana wt control plants and PG57 and PG26 transgenic lines overexpressing the AtPrx71 gene.
2016-01-06 | E-GEOD-66980 | biostudies-arrayexpress
Project description:Transcriptional profiling after inhibition of cellulose synthesis by thaxtomin A and isoxaben in Arabidopsis thaliana suspension cells Perturbations in the cellulose content of the plant cell wall lead to global modifications in cellular homeostasis, as seen in cellulose synthase mutants or after inhibiting cellulose synthesis. In particular, application of inhibitors of cellulose synthesis such as thaxtomin A (TA) and isoxaben (IXB) initiates a programmed cell death (PCD) in Arabidopsis thaliana suspension cells that is dependent on de novo gene transcription. To further understand how TA and IXB activate PCD, a whole genome microarray analysis was performed on mRNA isolated from Arabidopsis suspension cells exposed to TA and IXB. More than 75% of the genes upregulated by TA were also upregulated by IXB, including genes encoding cell wall-related and calcium-binding proteins, defence/stress-related transcription factors, signalling components and cell death-related proteins. Comparisons with published transcriptional analyses revealed an important subset of genes generally induced in response to various biotic and abiotic stress.
2009-08-27 | GSE17824 | GEO
Project description:The cell wall is a crucial structure in plant cells, and modifications in its composition often have a major impact on growth and development. However, the molecular mechanisms responsible for the negative effects of cell wall alterations on plant growth are largely unknown. It was previously shown that a reduction in the levels of de-esterified homogalacturonan, a major pectin component of cell walls, in Arabidopsis thaliana plants expressing a fungal polygalacturonase or mutated in the QUASIMODO2 gene (qua2-1 plants), cause severe growth defects. Here we show that the class III peroxidase AtPrx71 is strongly up-regulated in these plants, as well as in response to alterations of other wall structural components, including treatments the cellulose synthase inhibitor isoxaben. Analysis of atprx71 loss-of-function mutants and of plants overexpressing AtPrx71 indicates that this gene negatively affects Arabidopsis growth at different stages of development. Furthermore, lack of AtPrx71 partially suppresses the dwarf phenotype of qua2-1, suggesting that this protein contributes to the growth defects observed in plants undergoing cell wall damage. AtPrx71 appears to promote the production of reactive oxygen species in qua2-1 plants, as well as in plants treated with isoxaben. We propose that production of reactive oxygen species mediated by AtPrx71 negatively regulates Arabidopsis growth both during physiological development and in response to loss of cell wall integrity.
2016-01-06 | GSE66980 | GEO
Project description:Transcriptome analysis of isoxaben-induced loss of cell wall integrity in Arabidopsis seedling liquid culture
| PRJNA429347 | ENA
Project description:Transcriptome analysis of isoxaben-induced loss of cell wall integrity in Arabidopsis nia1/2 mutant
| PRJNA431488 | ENA
Project description:Transcriptional profiling after inhibition of cellulose synthesis by thaxtomin A and isoxaben in Arabidopsis thaliana suspension cells; Perturbations in the cellulose content of the plant cell wall lead to global modifications in cellular homeostasis, as seen in cellulose synthase mutants or after inhibiting cellulose synthesis. In particular, application of inhibitors of cellulose synthesis such as thaxtomin A (TA) and isoxaben (IXB) initiates a programmed cell death (PCD) in Arabidopsis thaliana suspension cells that is dependent on de novo gene transcription. To further understand how TA and IXB activate PCD, a whole genome microarray analysis was performed on mRNA isolated from Arabidopsis suspension cells exposed to TA and IXB. More than 75% of the genes upregulated by TA were also upregulated by IXB, including genes encoding cell wall-related and calcium-binding proteins, defence/stress-related transcription factors, signalling components and cell death-related proteins. Comparisons with published transcriptional analyses revealed an important subset of genes generally induced in response to various biotic and abiotic stress. Experiment Overall Design: TA, IXB and methanol (control) were added to Arabidopsis thaliana suspension cells three days after sub-culture. Cells were harvested for RNA isolation and frozen in liquid nitrogen after 6 hours of contact with the inhibitors. Samples consisted of four replicates for each condition. A total of 12 Affymetrix GeneChips® were used in this study, which correspond to 12 RNA samples from the four biological replicates for each of the TA, IXB or methanol addition.
2009-09-15 | E-GEOD-17824 | biostudies-arrayexpress
Project description:We are interested in understanding how plants respond to cell wall stress. The stress is created through inhibition of cellulose biosynthesis. Isoxaben is a drug that inhibits cellulose biosynthesis in a dose dependent manner. We used a concentration of 600 nM isoxaben which should inhibit appr. 80% of cellulose biosynthesis. We performed a time course experiment where seedlings were treated for 36h with isoxaben and in parrallel untreated seedlings were grown. At 8 different timepoints treated and untreated samples were harvested.
2008-01-08 | E-MEXP-711 | biostudies-arrayexpress
Project description:ra03-04_elongation_isoxaben - isoxaben treatment - 1. Study the molecular basis of the growth acceleration observed in hypocotyl cells. We previously have observed that cell elongation takes place in two distinct phases (Refregier et al., 2004). A slow growth phase during which a thick polylamellated wall is deposited and a rapid growth phase during which cell wall polymers are extensively remodelled. In dark-grown hypocotyls the slow growth phase takes place during the first 48h after seed-imbibition synchronously in all cells. At 48h after imbibition, cells at the basis of the hypocotyl undergo a growth acceleration, this acceleration follows an acropetal gradient along the hypocotyl. In this experiment, we investigated the changes in transcript abundance that accompany this sudden increase in growth rate. 2. Study the feed-back mechanisms involved in the coordination between cellulose synthesis and the cell elongation. The inhibition of cellulose using chemical inhibitors also inhibits cell elongation. In the same study (Refregier et al., 2004), we have observed that the effect of the cellulose synthesis inhibitor isoxaben on cell elongation is different dependent on the growth stage. When applied during the slow growth phase, cells continue to elongate slowly and do not show the growth acceleration at 48h after imbibition. Surprisingly, when applied after the growth acceleration, isoxaben does not inhibit subsequent growth. In this study we compared the effects of isoxaben on the transcript profiles before and after the growth acceleration. This should inform us about the response of the hypocotyl cells to the inhibition of cellulose and should provide insights into the molecular events that underly the observed coupling between cellulose synthesis and cell elongation. - 1- 45 hours, transfer to medium +/-isoxaben, harvest at 48 hours: comparison 48 hours + /- isoxaben. 2- 52 hours, transfer on + /-isoxaben, harvest 55 hours: comparison 55 hours + /-isoxaben (after transition: inhibition synthesis of cellulose, no inhibition of cellular elongation). Keywords: treated vs untreated comparison
2007-06-20 | GSE7985 | GEO
Project description:The remarkable desiccation tolerance of the vegetative tissues in the resurrection species Craterostigma plantagineum (Hochst.) is favored by its unique cell wall folding mechanism that allows the ordered and reversible shrinking of the cells without damaging neither the cell wall nor the underlying plasma membrane. The ability to withstand extreme drought is also maintained in abscisic acid pre-treated calli, which can be cultured both on solid and in liquid culture media. Cell wall research has greatly advanced thanks to the use of inhibitors affecting the biosynthesis of e.g. cellulose, since they allowed the identification of the compensatory mechanisms underlying habituation. Considering the innate cell wall plasticity of C. plantagineum, the goal of this investigation was to understand whether habituation to the cellulose biosynthesis inhibitors dichlobenil and isoxaben entailed or not identical mechanisms as known for non-resurrection species and to decipher the cell wall proteome of habituated cells. The results showed that exposure of C. plantagineum calli/cells triggered abnormal phenotypes as reported in non-resurrection species. Additionally, the data demonstrated that it was possible to habituate Craterostigma cells to dichlobenil and isoxaben and that gene expression and proteomics did not follow the same trend. Shotgun and gel-based proteomics revealed a common set of proteins induced upon habituation, but also identified candidates solely induced by habituation to one of the two inhibitors. Finally, it is hypothesized that alterations in auxin levels are responsible for the increased abundance of cell wall-related proteins upon habituation.
2022-02-17 | PXD026723 | Pride