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Phosphate excess increases susceptibility to pathogen infection in rice

ABSTRACT: Phosphate excess increases susceptibility to pathogen infection in rice

PROVIDER: PRJNA566419 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10148700_1.fastq.gz	Fastqsanger.gz
	SRR10148700_2.fastq.gz	Fastqsanger.gz
	SRR10148701_1.fastq.gz	Fastqsanger.gz
	SRR10148701_2.fastq.gz	Fastqsanger.gz
	SRR10148702_1.fastq.gz	Fastqsanger.gz

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Phosphate excess increases susceptibility to pathogen infection in rice

Project description:Phosphorus (P) is an essential nutrient for plant growth and productivity. Due to soil fixation, however, phosphorus availability in soil is rarely sufficient to sustain high crop yields. Fertilizers are widely used to circumvent the limited bioavailability of phosphate (Pi) which led to a scenario of excessive soil P in agricultural soils. Whereas adaptive responses to Pi deficiency have been deeply studied, less is known about how plants adapt to Pi excess and how Pi excess might affect disease resistance. Here, we show that high Pi fertilization in rice plants, and subsequent Pi accumulation in leaves, enhances susceptibility to infection by Magnaporthe oryzae, the causal agent of the rice blast disease. Equally, MIR399f overexpression causes an increase in Pi content in rice leaves which results in enhanced susceptibility to M. oryzae. During pathogen infection, a weaker activation of defense-related genes occurs in rice plants accumulating Pi in leaves, a response that is in agreement with the phenotype of blast susceptibility observed in these plants. These data support that Pi, when in excess, compromises defense mechanisms in rice while demonstrating that miR399 functions as a negative regulator of rice immunity. The two signaling pathways, Pi signaling and defense signaling, must operate in a coordinated manner in controlling disease resistance. This information provides a basis to understand the molecular mechanisms involved in immunity in rice plants grown under a high Pi fertilization regime, an aspect that should be considered in management of the rice blast disease

2020-03-16 | GSE137735 | GEO

Phosphate excess increases susceptibility to pathogen infection in rice.

Project description:Phosphorus (P) is an essential nutrient for plant growth and productivity. Due to soil fixation, however, phosphorus availability in soil is rarely sufficient to sustain high crop yields. The overuse of fertilizers to circumvent the limited bioavailability of phosphate (Pi) has led to a scenario of excessive soil P in agricultural soils. Whereas adaptive responses to Pi deficiency have been deeply studied, less is known about how plants adapt to Pi excess and how Pi excess might affect disease resistance. We show that high Pi fertilization, and subsequent Pi accumulation, enhances susceptibility to infection by the fungal pathogen Magnaporthe oryzae in rice. This fungus is the causal agent of the blast disease, one of the most damaging diseases of cultivated rice worldwide. Equally, MIR399f overexpression causes an increase in Pi content in rice leaves, which results in enhanced susceptibility to M. oryzae. During pathogen infection, a weaker activation of defence-related genes occurs in rice plants over-accumulating Pi in leaves, which is in agreement with the phenotype of blast susceptibility observed in these plants. These data support that Pi, when in excess, compromises defence mechanisms in rice while demonstrating that miR399 functions as a negative regulator of rice immunity. The two signalling pathways, Pi signalling and defence signalling, must operate in a coordinated manner in controlling disease resistance. This information provides a basis to understand the molecular mechanisms involved in immunity in rice plants under high Pi fertilization, an aspect that should be considered in management of the rice blast disease.

| S-EPMC7060143 | biostudies-literature

Global gene expression of Ruegeria pomeroyi DSS-3 during ammonium-limited, ribose phosphate-, methylphosphonate-, or potassium phosphate-excess growth regimes or during potassium phosphate-limited, ammonium-excess regime

Project description:We used the previously designed oligonucleotide microarrays (BM-CM-<rgmann et al., 2007, Environmental Microbiology, 9: 2742-2755) to detect the mRNA transcripts of R. pomeroyi DSS-3 when the cells were cultured under steady-state conditions limited with ammonium (NH4Cl, 0.26 mM) but with an excess of D-ribose-5-phosphate (C5H9Na2O8P*2H2O, 0.5 mM), methylphosphonic acid (CH5PO3, 0.5 mM), or potassium phosphate (KH2PO4, 0.5 mM), or during ammonium excess (NH4Cl, 2.8 mM) but were limited with potassium phosphate (KH2PO4, 9.2 M-NM-<M). A total of 13 microarray hybridizations were performed: three biological replicates each from ribose phosphate, methylphosphonate, or potassium phosphate excess growth regimes, three biological replicates from potassium phosphate limited growth regime, and one technical replicate for the potassium phosphate excess growth regime. Data for the technical replicates were averaged and combined, resulted in a total of 12 samples.

2014-06-02 | E-GEOD-38740 | biostudies-arrayexpress

Project description:We used the previously designed oligonucleotide microarrays (Bürgmann et al., 2007, Environmental Microbiology, 9: 2742-2755) to detect the mRNA transcripts of R. pomeroyi DSS-3 when the cells were cultured under steady-state conditions limited with ammonium (NH4Cl, 0.26 mM) but with an excess of D-ribose-5-phosphate (C5H9Na2O8P*2H2O, 0.5 mM), methylphosphonic acid (CH5PO3, 0.5 mM), or potassium phosphate (KH2PO4, 0.5 mM), or during ammonium excess (NH4Cl, 2.8 mM) but were limited with potassium phosphate (KH2PO4, 9.2 μM).

2014-06-02 | GSE38740 | GEO

A Comparative Study of Global Transcriptomic Responses under Excess or deficient Phosphate (Pi) Regime reveals ethylene mediated signaling in Arabidopsis.

Project description:Phosphorus is an essential macronutrient element, but some time causes problems if present in excess. Unlike the enormous molecular and morphophysiological information available in plants regarding phosphate (Pi) deficiency, little is known about the effect of excess Pi on plants, which is indeed essential for its remediation. Here, we have carried out a comparative study of plant molecular responses under excess Pi (20 mM) or without Pi (0 mM) at transcriptome level. The 1.25 mM treatment concentration of Pi used as a control to obtain differentially regulated genes under above mentioned Pi regimes. A novel whole-transcript expression array, i.e. Arabidopsis Gene 1.0 ST Array, was used to perform these experiments. The most distinctly regulated groups of genes represent modulation in ethylene mediated signaling, Fe deficiency response, and root development. We have also identified some defensin like genes, possessing a gibberellic acid regulated domain (GASA like) under excess Pi treatment. Overall, this study will not only help in dissecting the mechanism of plant responses under excess Pi but also provide the clues about the unknown genes involved in phosphorus homeostasis.

2017-06-23 | GSE66925 | GEO

Whole genome RNA-sequencing from roots of Arabidopsis thaliana wild-type and stop1 exposed to low pH, low phosphate (Pi), Aluminum and Iron excess conditions.

Project description:Total mRNA was extracted from the root tips (10 mm from the root apex) of wild-type plants (Col-0 accession) and stop1 mutants grown 5 days after germination under optimum conditions and then transferred for 16 hours to low phosphate(Pi), low pH, Al and Fe excess mediums.

2020-10-07 | GSE148457 | GEO

Progesterone increases metabolism via the pentose phosphate pathway in bovine uterine epithelial cells

Project description:During early pregnancy, glucose is essential for the uterine epithelium and the developing embryo. In cows, studies have shown that progesterone increases the secretion of glucose into the uterine lumen. Nevertheless, how progesterone affects glucose metabolism in the uterine epithelium has been sparsely investigated. Therefore, our objective was to investigate how progesterone influences glucose metabolism in immortalized bovine uterine epithelial (BUTE) cells. Progesterone treatment (10 μM) increased glucose consumption. To gain a more global picture of the effects of progesterone, RNAseq was performed after BUTE cells were treated with vehicle (DMSO) or 10 μM for 24 hours. KEGG analysis indicated that progesterone altered genes associated with metabolic pathways and glutathione metabolism. Manually examining genes unique to specific glucose metabolic pathways identified an increase in the rate-limiting enzyme in the pentose phosphate pathway—glucose-6-phosphate dehydrogenase. Functionally, a major product of the pentose phosphate pathway is NADPH, and progesterone treatment increased NADPH concentrations in BUTE cells. In cows, immunohistochemistry confirmed that glucose-6-phosphate dehydrogenase levels were higher in the uterine epithelium in the luteal phase when progesterone concentrations are high. In conclusion, progesterone increased glucose-6-phosphate dehydrogenase expression and metabolism via the pentose phosphate pathway in the bovine uterine epithelium. This metabolism could provide substrates for cell proliferation, molecules to be secreted into the uterine lumen that supports embryonic development, or maintain reduction/oxidation balance in the uterine epithelium.

2024-10-09 | GSE269076 | GEO

Single Cell Multi-Omics of Human Preimplantation Embryos Demonstrates Susceptibility to Excess Glucocorticoid Exposure

Project description:Single Cell Multi-Omics of Human Preimplantation Embryos Demonstrates Susceptibility to Excess Glucocorticoid Exposure

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Phosphate Starvation Signaling Increases Mitochondrial Membrane Potential through Respiration-independent Mechanisms

Project description:The mitochondrial membrane potential directly powers many critical functions of mitochondria, including ATP production, mitochondrial protein import, and metabolite transport. Its loss is a cardinal feature of aging and mitochondrial diseases, and cells closely monitor membrane potential as an indicator of mitochondrial health. Given its central importance, it is logical that cells would modulate mitochondrial membrane potential in response to demand and environmental cues, but there has been little exploration of this question. We report that loss of the Sit4 protein phosphatase in yeast increases mitochondrial membrane potential mostly by inducing the expression of the electron transport chain but also activates the phosphate starvation response. Indeed, a similarly elevated mitochondrial membrane potential is also elicited by either phosphate starvation or by abrogation of the Pho85-dependent phosphate sensing pathway. This enhanced membrane potential is primarily driven by an unexpected activity of the ADP/ATP carrier. We also demonstrate that this connection between phosphate limitation and enhancement of the mitochondrial membrane potential is evolutionarily conserved as it also is observed in primary and immortalized mammalian cells as well as in Drosophila. These data suggest that the mitochondrial membrane potential is subject to environmental stimuli and intracellular signaling regulation and raise the possibility for therapeutic enhancement even under conditions of mitochondrial dysfunction.

2024-02-15 | PXD037405 | Pride

IL-34 deficiency impairs FOXP3+ Treg function and increases susceptibility to diseases

Project description:IL-34 deficiency impairs FOXP3+ Treg function and increases susceptibility to diseases

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