Project description:Plant-parasitic cyst nematodes induce the formation of hypermetabolic feeding sites, termed syncytia, as their sole source of nutrients. The formation of the syncytium is orchestrated by the nematode in part by modulation of phytohormone responses, including cytokinin. In response to infection by the nematode H. schachtii, cytokinin signaling is transiently induced at the site of infection and in the developing syncytium. Arabidopsis lines with reduced cytokinin sensitivity show reduced susceptibility to nematode infection, indicating that cytokinin signaling is required for optimal nematode development. Furthermore, lines with increased cytokinin sensitivity also exhibit reduced nematode susceptibility. To ascertain why cytokinin hypersensitivity reduces nematode parasitism, we examined the transcriptomes in wild-type and a cytokinin-hypersensitive type-A arr Arabidopsis mutant in response to H. schachtii infection. Genes involved in the response to biotic stress and defense response were elevated in the type-A arr mutant in the absence of nematodes and were hyper-induced following H. schachtii infection, which suggests that the Arabidopsis type-A arr mutants impede nematode development because they are primed to respond to pathogen infection. These results suggest that cytokinin signaling is required for optimal H. schachtii parasitism of Arabidopsis, but that elevated cytokinin signaling triggers a heightened immune response to nematode infection.
Project description:Successful subversion of translation initiation factors 4E and 4G determines the infection success of potyviruses, the largest group of viruses affecting plants. Functional redundancy among these factors allows to engineer resistances through their genetic inactivation, however recent findings indicate that this strategy may be deleterious for the plant health and virus susceptibility. Here, we explored the cause of these adverse effects by studying the role of the Arabidopsis eIF4E1, which inactivation was previously reported not only to confer plant virus resistance, but also to induce increased susceptibility to the potyvirus turnip mosaic virus (TuMV). We report that eIF4E1 is required to maintain the global plant translational activity and to restrict TuMV accumulation during infection, as its absence is associated with a favoured virus multiplication over host translation.
Project description:There is mounting evidence for the role of epigenetic processes in the regulation of plant responses to a wide range of external stimuli. Despite their importance, the significance of epigenetic processes in plant-pathogen interactions remain poorly understood. So far, the role of histone modifications has not been investigated at genome wide level in plant-nematode interactions, although their expression levels are altered in nematode-induced galls. In this study, we first applied chemical inhibitors of histone modifying enzymes on rice plants. Despite theirdistinct effects on histone modifications, application of different concentrations of Niconinamide, sulfamethazine and fumaric acid lead to reduced susceptibility to nematode infection. Similarly, two overexpression lines of histone lysine methyltransferases and one histone deacetylase were analyzed in an infection assay with nematodes, showing contrasting results in susceptibility. These data indicate that histone modifications can affect plant defence against nematodes in rice. To further investigate their effect, the genome-wide level of three histone marks namely H3K9ac, H3K9me2 and H3K27me3 was studied by chromatin-immunoprecipitation (ChIP)-sequencing on nematode-induced galls in comparison with control root tips.
Project description:Plant-parasitic cyst nematodes induce syncytial cells in the roots of their host plants. Cyst nematodes are sexually dimorphic, with their differentiation into male or femaleis strongly influenced by host environmental conditions. Under favorable conditions with plenty of nutrients, more females develop, whereas mainly male nematodes develop under adverse conditions, such as in resistant plants. We collected root segments containing male-associated syncytia (MAS) or female-associated syncytia (FAS), isolated syncytial cells by laser microdissection, and performed a comparative transcriptome analysis using Microarrays.
Project description:Background: Epigenetic processes play an important role in the plant response to adverse environmental conditions. A role for DNA hypomethylation has recently been suggested in the pathogenic interaction between bacteria and plants, yet it remains unclear whether this phenomenon reflects a conserved and general plant immunity response. We therefore investigated the role of DNA methylation in the plant defence against damaging parasitic nematodes. Methods and results: Treatment of roots of rice (monocot plant) and tomato (dicot plant) by a nematode-associated molecular pattern (NAMP) from different parasitic nematodes revealed global DNA hypomethylation using ELISA based quantification, suggesting conservation among plants. Focusing on root-knot induced gall tissue in rice, the causal impact of hypomethylation on immunity was revealed by a significantly reduced plant susceptibility upon 5-Azacitidine treatment. Whole genome bisulfite sequencing revealed that hypomethylation was massively present in the CHH context, while absent for CpG or CHG nucleotide contexts. CHH hypomethylated regions were predominantly associated with gene promoter regions, which was not correlated with activated gene expression at the same time point, but rather showed a delayed effect on transcriptional gene activation. Finally, the relevance of CHH hypomethylation in plant defence was confirmed in rice mutants of the RNA-directed DNA methylation pathway (RdDM) and DDM1, which are known to be steering DNA methylation in CHH context. Conclusions: We demonstrated that DNA hypomethylation confers enhanced defence in rice towards root-parasitic nematodes and is likely to be part of the basal NAMP-triggered immunity response in plants.
Project description:deOliveiraDalMolin2010 - Genome-scale
metabolic network of Arabidopsis thaliana (AraGEM)
This model is described in the article:
AraGEM, a genome-scale
reconstruction of the primary metabolic network in
Arabidopsis.
de Oliveira Dal'Molin CG, Quek LE,
Palfreyman RW, Brumbley SM, Nielsen LK.
Plant Physiol. 2010 Feb; 152(2):
579-589
Abstract:
Genome-scale metabolic network models have been successfully
used to describe metabolism in a variety of microbial organisms
as well as specific mammalian cell types and organelles. This
systems-based framework enables the exploration of global
phenotypic effects of gene knockouts, gene insertion, and
up-regulation of gene expression. We have developed a
genome-scale metabolic network model (AraGEM) covering primary
metabolism for a compartmentalized plant cell based on the
Arabidopsis (Arabidopsis thaliana) genome. AraGEM is a
comprehensive literature-based, genome-scale metabolic
reconstruction that accounts for the functions of 1,419 unique
open reading frames, 1,748 metabolites, 5,253 gene-enzyme
reaction-association entries, and 1,567 unique reactions
compartmentalized into the cytoplasm, mitochondrion, plastid,
peroxisome, and vacuole. The curation process identified 75
essential reactions with respective enzyme associations not
assigned to any particular gene in the Kyoto Encyclopedia of
Genes and Genomes or AraCyc. With the addition of these
reactions, AraGEM describes a functional primary metabolism of
Arabidopsis. The reconstructed network was transformed into an
in silico metabolic flux model of plant metabolism and
validated through the simulation of plant metabolic functions
inferred from the literature. Using efficient resource
utilization as the optimality criterion, AraGEM predicted the
classical photorespiratory cycle as well as known key
differences between redox metabolism in photosynthetic and
nonphotosynthetic plant cells. AraGEM is a viable framework for
in silico functional analysis and can be used to derive new,
nontrivial hypotheses for exploring plant metabolism.
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