Transcriptome analysis of isoxaben-induced loss of cell wall integrity in Arabidopsis nia1/2 mutant
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ABSTRACT:
ORGANISM(S): Arabidopsis thaliana
PROVIDER: GSE109613 | GEO | 2018/01/25
REPOSITORIES: GEO
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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:The fungal cell wall provides protection and structure to cells, and serves as an important target for antifungal compounds. The cell wall integrity (CWI) signaling pathway regulates the transcriptional response to various cell wall stresses, but emerging evidence suggests posttranscriptional pathways play an important complementary role. Here, we show that the RNA-binding proteins (RBPs) Mrn1 and Nab6 specifically target the 3′ UTRs of a largely overlapping set of cell wall-associated mRNAs. These mRNAs are downregulated in the absence of Nab6, indicating that Nab6 directly or indirectly stabilizes its target mRNAs. We further show that Nab6 acts in parallel to conventional CWI signaling to maintain adequate expression of cell wall mRNAs. Cells lacking both pathways are hypersensitive to antifungal compounds targeting the cell wall, while deletion of MRN1 partially alleviates the growth and molecular phenotypes associated with the Dnab6 strain. Taken together, our results uncover a novel posttranscriptional pathway which mediates resistance to cell wall stress and antifungal compounds.
2023-02-03 | GSE210558 | GEO
Project description:The structure and composition of plant cell walls are modified to accommodate the needs of the cell and in response to environmental stimuli. Growth, development, and defense may demand potentially conflicting functional cell wall requirements, and thus modifications of the cell wall are tightly controlled in an adaptive manner. These modifications are mediated by a dedicated cell wall integrity (CWI) maintenance mechanism. We investigated the responses to cell wall damage (CWD) that compromise CWI and the underlying mechanisms in Arabidopsis thaliana. Inhibitor- and enzyme-triggered CWD induced similar, turgor-sensitive stress responses. Genetic analysis showed that the receptor-like kinase (RLK) FEI2 and the plasma membrane-localized mechano-sensitive Ca2+- channel MCA1 function downstream of the RLK THE1 in CWD perception. Phenotypic clustering with 27 genotypes identified a core group of RLKs and ion channels required for activation of CWD responses. In contrast, the responses were repressed by pattern-triggered immunity (PTI) signaling components including the receptors for plant elicitor peptides (AtPeps) PEPR1 and PEPR2 (PEPR1/2). Application of AtPep1 and AtPep3 repressed CWD-induced phytohormone accumulation in a concentration dependent manner. CWD induced the expression of both PROPEP1 and PROPEP3 as well as the release of a PROPEP3 fusion protein into the growth medium. These results suggest that AtPep-mediated signaling suppresses CWD-induced defense responses. If key PTI signaling elements acting downstream of PEPR1/2 are dysfunctional, suppression of CWD-induced responses is alleviated, thus compensating for the impairment.
2018-07-03 | PXD009153 | Pride
Project description:The Neurospora crassa GUL-1 is part of the COT-1 pathway, which plays key roles in regulating polar hyphal growth and cell wall remodeling. We show that GUL-1 is a bona fide mRNA binding protein (RBP) that can associate with 828 “core” mRNA species. When cell wall integrity (CWI) is challenged, the repertoire of associated RNA species increases up to 2628 mRNAs (including its own transcript). GUL-1 can bind mRNAs of genes related to translation, cell wall remodeling, circadian clock, endoplasmatic reticulum (ER), as well as CWI and osmoregulatory response MAPK pathway components. GUL-1 interacts with over 100 different proteins, including stress granule proteins, components of the translational and cell wall remodeling machinery, as well as ER components and those of the MAPK, COT-1 and STRIPAK complexes. Several additional RBPs were also shown to physically interact with GUL-1. We demonstrate that under stress conditions GUL-1 can localize to the ER and that GUL-1 affects the CWI pathway as is evident via altered phosphorylation levels of MAK-1, interaction with mak-1 transcript and involvement in the expression level of the transcription factor adv-1. Taken together, we suggest that the RBP GUL-1 functions in multiple cellular processes, including the regulation of cell wall remodeling. The latter is mechanistically concerted with the MAK-1 pathway in a stress-related manner. Methods: In this study we show that GUL-1 is a bona fide mRNA binding protein (RBP) that associates with different mRNAs, including its own transcript, as determined by RNA antisense purification and RNA immunoprecipitation experiments. Results: We demonstrate that GUL-1 may physically interact with multiple proteins included translation processes, cell wall remodeling and cell wall integrity (CWI). We show that GUL-1 affects the CWI pathway as is evident via altered phosphorylation levels of MAK-1, interaction with mak-1 transcript and involvement in the expression level of the transcription factor adv-1. Conclusions:We suggest that the RBP GUL-1 functions in the regulation of cell wall remodeling in concert with the MAK-1 pathway in a stress-related manner.
2021-04-14 | GSE152935 | 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
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:As a dynamic structure with a barrier between the cell and the outside world, maintenance of cell wall integrity (CWI) is important for fungal growth, development and pathogenicity processes. Here we characterized a MADS-box transcription factor RlmA (AoRlmA) downstream of the CWI regulatory pathway in the nematode-trapping fungus Arthrobotrys oligospora. Deletion of AorlmA caused a reduction in mycelial growth and the number of nuclei, and significant downregulation of transcript levels of genes related to nucleus synthesis and DNA damage repair, such as rad3, spo11, and rad25. Meanwhile, the ΔAorlmA mutant strains showed a significant reduction in spore production compared with the wild-type (WT) strain, and the transcript levels of sporulation-related genes was downregulated in the ΔAorlmA mutant during the early and middle stages of condiation, such as flbA, medA, and vosA. Meanwhile, the mycelial cell wall of the ΔAorlmA mutant strain showed breakage. Also, the transcript levels of genes related to cell wall synthesis were significantly down-regulated in the mutant strain compared to the WT strain, and the mutant strain was more sensitive to stresses of cell wall synthesis disruptors, oxidative stress and osmotic stress than the WT strain. Compared with the WT strain, the ΔAorlmA mutant strain not only had a reduced number of traps and nematicidal ability, but also, the shape of the traps of the mutants has also changed. In addition, In addition, AoRlmA also regulates autophagy and endocytosis. Transcriptome analysis of ΔAorlmA mutant strains showed that AorlmA regulates redox, cell wall synthesis, DNA replication and damage repair, and pathogenic processes. Metabolomic analysis showed that AorlmA is involved in the biosynthesis of secondary metabolites of A. oligospora. To summarise, our data suggest that AorlmA is involved in growth, sporulation, spore germination, maintenance of cell wall integrity, DNA replication and damage repair, pathogenesis, autophagy and secondary metabolite biosynthesis processes.
2023-06-25 | GSE207080 | GEO
Project description:Cellulose is the major polysaccharide in the primary and secondary cell wall. Its breakdown generates short-chain cellooligomers (COs) which induce Ca2+-dependent cell wall integrity (CWI) responses. Recently, a mutant (cork1) which did not respond to COs was identified. To find out the early phosphorylation events following CO perception, roots of the segregated wild-type and homozygous mutants (F2 generation from cork1-2 X AeqWT) were treated with 10 µM cellotriose or water for 0, 5 and 15 minutes. Phosphoproteome analyses identified early targets involved in signaling, the endoplasmatic recticulum/Golgi secretory pathway, cell wall repair and immune responses. The result identified protein targets of the novel CO-CORK1 pathway and shine light on the role of COs in CWI maintenance.
2022-09-23 | PXD033224 | Pride
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.
2014-07-01 | GSE57217 | GEO
Project description:Transcriptome analysis of isoxaben-induced loss of cell wall integrity in Arabidopsis nia1/2 mutant
| PRJNA431488 | ENA