Transcriptome analysis of isoxaben-induced loss of cell wall integrity in Arabidopsis seedling liquid culture
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ABSTRACT:
PROVIDER: PRJNA429347 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6456400.fastq.gz | Fastqsanger.gz | |||
| SRR6456401.fastq.gz | Fastqsanger.gz | |||
| SRR6456392.fastq.gz | Fastqsanger.gz | |||
| SRR6456402.fastq.gz | Fastqsanger.gz | |||
| SRR6456393.fastq.gz | Fastqsanger.gz |
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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:Transcriptome analysis of isoxaben-induced loss of cell wall integrity in Arabidopsis nia1/2 mutant
| PRJNA431488 | ENA
Project description:Chitin is an important fungal cell wall component that is cross-linked to β-glucan for structural integrity. Acquisition of chitin to glucan cross-links has previously been shown to be performed by transglycosylation enzymes in S. cerevisiae, called Congo Red hypersensitive (Crh) enzymes. Here, we characterized the impact of deleting all seven gene members of the crh gene family (crhA-G) in Aspergillus niger on cell wall integrity, cell wall composition and genome-wide gene expression. In this study, we show that the seven-fold knockout strain shows slightly compact plate growth, but no increased sensitivity to cell wall perturbing compounds. Additionally, we found that the cell wall composition of this knockout strain was virtually identical to that of the wild type. In congruence with these data, genome-wide expression analysis revealed very limited changes in gene expression and no signs of activation of the cell wall integrity response pathway. However, deleting the entire crh gene family in cell wall mutants that are deficient in either galactofuranose (ΔugmA) or α-glucan (ΔagsE and ΔagsA, ΔagsE), resulted in a synthetic growth defect and an increased sensitivity towards Congo Red compared the parental strains. Altogether, these results indicate that loss of the crh gene family in A. niger does not trigger the cell wall integrity response in itself, but does play an important role in ensuring cell wall integrity in mutant strains with reduced galactofuranose or α-glucan.
2019-12-21 | GSE142461 | 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: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:Plant cell walls maintain their functional integrity during growth, defense and turgor generation through a dedicated cell wall integrity (CWI) maintenance mechanism. Upon detection of integrity impairment due to cell wall damage (CWD) compensatory responses are activated to maintain CWI. Responses include production of salicylic acid (SA), jasmonic acid (JA) and lignin as well as growth inhibition. Here we investigated the processes responsible for inducing growth inhibition upon CWD in Arabidopsis thaliana seedlings. Genetic studies implicated NITRATE REDUCTASE1 2 (NIA1 2) in the response to CWD. RNAseq-based transcriptomics showed that nearly all the CWD-induced transcript changes detectable in Col-0 were absent in nia1 2 seedlings.
2018-01-25 | GSE109613 | 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
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.
2021-11-03 | PXD026733 | Pride
Project description:The cell wall is essential for viability of fungi and is an effective drug target in pathogens such as Candida albicans. The contribution of posttranscriptional gene regulators to cell wall integrity in C. albicans is unknown. We show that the C. albicans Ccr4-Pop2 mRNA deadenylase, a regulator of mRNA stability and translation, is required for cell wall integrity. The ccr4/pop2 mutants display reduced wall β-glucans and sensitivity to the echinocandin caspofungin. Moreover, the deadenylase mutants are compromised for filamentation and virulence. We demonstrate that defective cell walls in the ccr4/pop2 mutants are linked to dysfunctional mitochondria and phospholipid imbalance. To further understand mitochondrial function in cell wall integrity, we screened a Saccharomyces cerevisiae collection of mitochondrial mutants. We identify several mitochondrial proteins required for caspofungin tolerance and find a connection between mitochondrial phospholipid homeostasis and caspofungin sensitivity. We focus on the mitochondrial outer membrane SAM complex subunit Sam37, demonstrating it is required for both trafficking of phospholipids between the ER and mitochondria and cell wall integrity. Moreover, in C. albicans also Sam37 is essential for caspofungin tolerance. Our study provides the basis for an integrative view of mitochondrial function in fungal cell wall biogenesis and resistance to echinocandin antifungal drugs. Two-color experimental design comparing cells with a double-knockout of the CCR4 genes to cells with a reintegrated CCR4 gene.
2010-12-10 | E-GEOD-25891 | biostudies-arrayexpress
Project description:The cell wall is essential for viability of fungi and is an effective drug target in pathogens such as Candida albicans. The contribution of posttranscriptional gene regulators to cell wall integrity in C. albicans is unknown. We show that the C. albicans Ccr4-Pop2 mRNA deadenylase, a regulator of mRNA stability and translation, is required for cell wall integrity. The ccr4/pop2 mutants display reduced wall β-glucans and sensitivity to the echinocandin caspofungin. Moreover, the deadenylase mutants are compromised for filamentation and virulence. We demonstrate that defective cell walls in the ccr4/pop2 mutants are linked to dysfunctional mitochondria and phospholipid imbalance. To further understand mitochondrial function in cell wall integrity, we screened a Saccharomyces cerevisiae collection of mitochondrial mutants. We identify several mitochondrial proteins required for caspofungin tolerance and find a connection between mitochondrial phospholipid homeostasis and caspofungin sensitivity. We focus on the mitochondrial outer membrane SAM complex subunit Sam37, demonstrating it is required for both trafficking of phospholipids between the ER and mitochondria and cell wall integrity. Moreover, in C. albicans also Sam37 is essential for caspofungin tolerance. Our study provides the basis for an integrative view of mitochondrial function in fungal cell wall biogenesis and resistance to echinocandin antifungal drugs.
2010-12-10 | GSE25891 | GEO