Project description:Trichoderma spp. are filamentous fungi that colonize plant roots conferring beneficial effects to plants, indirectly through the induction of their defense systems or directly through the suppression of phytopathogens in the rhizosphere. Transcriptomic analyses of Trichoderma emerged as a powerful method for identifying the molecular events underlying the establishment of this beneficial relationship. Here, we focus on the transcriptomic response of Trichoderma virens during its interaction with Arabidopsis seedlings. The main response of T. virens to co-cultivation with Arabidopsis was the repression of gene expression. The biological processes of transport and metabolism of carbohydrates were downregulated, including a set of cell-wall-degrading enzymes putatively relevant for root-colonization. Repression of such genes reached their basal levels at later times of the interaction when genes belonging to the biological process of copper ion transport were induced, a necessary process providing copper as a cofactor for cell-wall degrading enzymes with auxiliary activities (AAs) class. RNA-Seq analysis showed the induction of a member of the SNF2 family of chromatin remodelers/helicase-related proteins, which was named IPA-1 (Increased Protection of Arabidopsis-1). Sequence analyses of IPA-1 showed as its closest relatives members of the Rad5/Rad16- and SNF2-subfamilies; however, it grouped into a different clade. Although deletion of ipa-1 in T. virens did not affect its growth, the antibiosis of Δipa-1 culture filtrates showed a diminished effect against Rhizoctonia solani but remained unaltered against Botrytis cinerea. Triggering of the plant defense genes in plants treated with Δipa-1 was higher, showing enhanced resistance against Pseudomonas syringae but not against B. cinerea as compared to wild type.
Project description:In this study we show that the Arabidopsis transcription factor MYB46, previously described to regulate secondary cell wall biosynthesis in the vascular tissue of the stem, is pivotal for mediating disease susceptibility to the fungal pathogen Botrytis cinerea. We identified MYB46 by its ability to bind to a new cis element located in the 5´ promoter region of the pathogen-induced Ep5C gene which encodes a type III cell wall-bound peroxidase. We present genetic and molecular evidence indicating that MYB46 modulates the magnitude of Ep5C gene induction following pathogenic insults. Moreover, we demonstrate that different myb46 knock-down mutant plants exhibit increased disease resistance to B. cinerea, a phenotype that is accompanied by selective transcriptional reprogramming of a set of genes encoding cell wall proteins and enzymes, of which extracellular type III peroxidases are conspicuous. In essence our results substantiates that defense-related signaling pathways and cell wall integrity are interconnected, and MYB46 likely functions as a disease susceptibility modulator to B. cinerea through the integration of cell wall remodeling and downstream activation of secondary lines of defense.
Project description:au10-13_cellwall - cell wall mutants - What is the impact of the loss of function of monolignol exporters? How does the plant cope with these transporters? Is there any compensation mechanism induced? What is the impact on lignin and cell wall biosynthesis? Does expression of a hydroxycinnamoyl-CoA hydratase/lyase in Arabidopsis stems generate a stress and affect genes involoved in cell wall biosynthesis? - Determine differentially expressed genes in stems of Arabidopsis plants lacking 2 monolignol exporter proteins. mRNA from stems of wild-type and transgenic 7-week-old plants grown in the same conditions were extracted and used for transcriptomic analysis. Three independant cultures were conducted for biological replicates. Determine differentially expressed genes in stems of Arabidopsis plants that express a hydroxycinnamoyl-CoA hydratase/lyase. mRNA from stems of wild-type and transgenic seven-week-old plants grown in the same conditions were extracted and used for transcriptomic analysis. Three independant cultures were conducted for biological replicates.
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.
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.