Transcriptome analysis of isoxaben-induced loss of cell wall integrity in Arabidopsis seedling liquid culture
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PROVIDER: PRJNA429347 | ENA |
REPOSITORIES: ENA
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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: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: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 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
Project description:A phosphoproteomic evaluation of the cellular response to micafungin (cell wall perturbant) in the filamentous fungi, A. nidulans, reveals putative, currently unknown cell wall integrity signaling (CWIS) associated proteins. This study used thirteen timepoints were taken from 0 to 10 minutes after cell wall exposure with two biological and two technical replicates. All data was processed using label free quantification with MaxQuant software.
2020-07-16 | PXD015038 | Pride
Project description:Transcriptome analysis of isoxaben-induced loss of cell wall integrity in Arabidopsis nia1/2 mutant
| PRJNA431488 | ENA
Project description:Dynamic study of the cell wall integrity signaling pathway in Aspergillus nidulans
| PRJNA562694 | ENA
Project description:Plants have evolved cell wall integrity signaling pathways to maintain cell wall homeostasis during rapid growth and in response to environmental stress. The cell wall leucine-rich repeat extensins LRX3/4/5, the RAPID ALKALINIZATION FACTOR (RALF) peptides RALF22/23, and FERONIA (FER) function as a module to regulate plant growth and salt stress responses via the sense of cell wall integrity. However, the intracellular signaling pathways that mediate the effects of the LRX3/4/5-RALF22/23-FER module are still largely unknown. Here, we report that jasmonic acid (JA), salicylic acid (SA), and abscisic acid (ABA) accumulate constitutively in lrx345 and fer mutants. Blocking JA pathway rescues the retarded growth phenotype of the lrx345 and fer-4 mutants, while disruption of ABA biosynthesis suppresses the salt-hypersensitivity of these mutants. Many salt stress-responsive genes display abnormal expression patterns in the lrx345 and fer-4 mutants, as well as in wild type plants treated with epigallocatechin gallate (EGCG), an inhibitor of pectin methylesterases, suggesting that the cell wall integrity is a critical factor that determines the expression of stress-responsive genes. Production of reactive oxygen species (ROS) is constitutively increased in the lrx345 and fer-4 mutants, and inhibition of ROS accumulation suppresses the salt-hypersensitivity of these mutants. Together, our results suggest that the LRX3/4/5-RALF22/23-FER module controls plant growth and salt stress responses by regulating hormonal homeostasis and ROS accumulation.
2021-07-15 | GSE136268 | GEO
Project description:Cryptococcus neoformans is a fungal pathogen of immunocompromised people that causes fatal meningitis. The fungal cell wall is essential to viability and pathogenesis of C. neoformans, and biosynthesis and repair of the wall is primarily controlled by the cell wall integrity (CWI) signaling pathway. Previous work by us and others have shown that deletion of genes encoding the four major kinases in the CWI signaling pathway, namely PKC1, BCK1, MKK2 and MPK1 results in severe cell wall phenotypes, sensitivity to a variety of cell wall stressors and, for Mpk1, reduced virulence in a mouse model. Here, we examined the global transcriptional response of gene deletions of BCK1, MKK2 and MPK1 compared to wild-type cells. We found over 1000 genes were differentially expressed in one or more of the deletion strains, with 115 genes differentially expressed in all three strains, many of which have been identified as genes regulated by the cAMP/protein kinase A (PKA) pathway. Biochemical measurements of cAMP levels in the kinase deletion stains revealed significantly less cAMP in all of the deletion strains compared to wild-type cells. The deletion strains also produced significantly smaller capsules than wild type KN99 under capsule inducing conditions, although they shed similar levels of capsule as wild type. Finally, addition of exogenous cAMP led to reduced sensitivity to cell wall stress and restored surface capsule to near wild-type levels. Thus, we have direct evidence of cross talk between the CWI and cAMP/PKA pathways that may have important implications for regulation of cell wall and capsule homeostasis. Comparison of three gene deletion strains to wild-type, with 3 biological replicates for each sample.
2014-07-01 | E-GEOD-57217 | biostudies-arrayexpress