Transcriptome analysis of isoxaben-induced loss of cell wall integrity in Arabidopsis nia1/2 mutant
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ABSTRACT:
PROVIDER: PRJNA431488 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6509880.fastq.gz | Fastqsanger.gz | |||
| SRR6509881.fastq.gz | Fastqsanger.gz | |||
| SRR6509882.fastq.gz | Fastqsanger.gz | |||
| SRR6509883.fastq.gz | Fastqsanger.gz | |||
| SRR6509884.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 seedling liquid culture
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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 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.
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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: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.
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Project description:Plant cells are surrounded by an extracellular cell wall that shields them from their abiotic and biotic environment. To coordinate their growth with their cell wall status, they have developed cell wall integrity mechanisms at the center of which lies the transmembrane Malectin-like receptor kinase FERONIA (FER). FER controls a myriad of plant developmental processes including sexual reproduction, cell growth and morphogenesis, often intersecting with phytohormones-dependent pathways such as abscisic acid (ABA) or plant immunity. Interestingly, FER and its downstream receptor-like cytoplasmic kinase MARIS (MRI) were shown to cooperate similarly in the control of root hair and rhizoid integrity for the vascular model Arabidopsis and the early diverging bryophyte model Marchantia polymorpha, respectively. Here, we carried out comparative transcriptomics and proteomics approach on Mpfer-1 and Mpmri-1 knock-down mutant plants and the wild-type strains Tak-1 and Tak-2. Our -omics analyses revealed that globally, MpFER and MpMRI largely cooperate to negatively regulate transcriptional and translational networks in particular those related to plant defense and ABA responses. Moreover, Mpfer-1 plants were found to be hypersensitive to ABA-dependent growth inhibition indicating that FER’s function of negatively regulating ABA-related growth responses is conserved between bryophytes and vascular plants.
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Project description:Plant cells are surrounded by an extracellular cell wall that shields them from their abiotic and biotic environment. To coordinate their growth with their cell wall status, they have developed cell wall integrity mechanisms at the center of which lies the transmembrane Malectin-like receptor kinase FERONIA (FER). FER controls a myriad of plant developmental processes including sexual reproduction, cell growth and morphogenesis, often intersecting with phytohormones-dependent pathways such as abscisic acid (ABA) or plant immunity. Interestingly, FER and its downstream receptor-like cytoplasmic kinase MARIS (MRI) were shown to cooperate similarly in the control of root hair and rhizoid integrity for the vascular model Arabidopsis and the early diverging bryophyte model Marchantia polymorpha, respectively. Here, we carried out comparative transcriptomics and proteomics approach on Mpfer-1 and Mpmri-1 knock-down mutant plants and the wild-type strains Tak-1 and Tak-2. Our -omics analyses revealed that globally, MpFER and MpMRI largely cooperate to negatively regulate transcriptional and translational networks in particular those related to plant defense and ABA responses. Moreover, Mpfer-1 plants were found to be hypersensitive to ABA-dependent growth inhibition indicating that FER’s function of negatively regulating ABA-related growth responses is conserved between bryophytes and vascular plants.
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Project description:The cell wall is a defining feature of plant cells and glues cells to each other. To overcome this physical constraint, plants must process and disconnect cell wall linkages during growth and development. However, little is known about the mechanism guiding cell-cell detachment and cell wall remodeling. Here, we identify two neighboring cell types in Arabidopsis that coordinate their activities to control cell wall processing, thereby ensuring precise abscission to discard organs. One cell type produces a honeycomb structure of lignin, which acts as a mechanical ‘brace’ to localize cell wall breakdown and spatially limit abscising cells. The second cell type undergoes transdifferentiation into epidermal cells, forming protective cuticle, demonstrating de novo specification of epidermal cells, previously thought to be restricted to embryogenesis. Loss of the lignin brace leads to inadequate cuticle formation, resulting in surface barrier defects and susceptible to infection. Altogether, we show how plants precisely accomplish abscission.
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