Transition metal-triggered immunity via an Arabidopsis NLR pair
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1232609 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR32587607_1.fastq.gz | Fastqsanger.gz | |||
| SRR32587607_2.fastq.gz | Fastqsanger.gz | |||
| SRR32587608_1.fastq.gz | Fastqsanger.gz | |||
| SRR32587608_2.fastq.gz | Fastqsanger.gz | |||
| SRR32587609_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 96 |
Similar Datasets
Project description:Plants growing in soil are challenged by multiple biotic (e.g. pathogens) and abiotic (e.g. heavy metals) stressors. Stress resistance is a key determinant for plants to thrive in the environment. Resistance to pathogens requires innate immunity 1, whereas tolerance to metal ions is accomplished by mechanisms such as complexation and compartmentation2,3. Some transition metals can enhance plant’s defense against pathogens4,5, but the mechanism remains unclear. Here, we show that an Arabidopsis head-to-head gene pair of intracellular nucleotide-binding leucine-rich repeat (NLR) receptors antagonistically control transition metal-triggered immunity. One NLR, STM2 directly perceives transition metal ions, such as Cd2+, Cu2+ and Zn2+, as a ligand to activate its NAD+ hydrolytic activity and immune responses, triggering enhanced resistance to the soil-borne bacterial wilt pathogen Ralstonia solanacearum. The other NLR, STM1 suppresses STM2 to protect plants from transition metal-triggered immunity and growth inhibition in the presence of excess metals. STM1 also dampens resistance to the pathogen. Our study defines an NLR activated by transition metals and reveals a trade-off between resistance to pathogens and tolerance to transition metals that are pervasive in soil.
2025-03-10 | GSE291114 | GEO
Project description:Plants growing in soil are challenged by multiple biotic (e.g. pathogens) and abiotic (e.g. heavy metals) stressors. Stress resistance is a key determinant for plants to thrive in the environment. Resistance to pathogens requires innate immunity , whereas tolerance to metal ions is accomplished by mechanisms such as complexation and compartmentation. Some transition metals can enhance plant’s defense against pathogens4,5, but the mechanism remains unclear. Here, we show that an Arabidopsis head-to-head gene pair of intracellular nucleotide-binding leucine-rich repeat (NLR) receptors antagonistically control transition metal-triggered immunity. One NLR, STM2 directly perceives transition metal ions, such as Cd2+, Cu2+ and Zn2+, as a ligand to activate its NAD+ hydrolytic activity and immune responses, triggering enhanced resistance to the soil-borne bacterial wilt pathogen Ralstonia solanacearum. The other NLR, STM1 suppresses STM2 to protect plants from transition metal-triggered immunity and growth inhibition in the presence of excess metals. STM1 also dampens resistance to the pathogen. Our study defines an NLR activated by transition metals and reveals a trade-off between resistance to pathogens and tolerance to transition metals that are pervasive in soil.
2025-03-11 | GSE291226 | GEO
Project description:Transition metal-triggered immunity via an Arabidopsis NLR pair
| PRJNA1231696 | ENA
Project description:Intracellular NLR receptors with a central nucleotide-binding domain allow plants to detect specific pathogen-secreted proteins and initiate immune signaling. A family of conserved Enhanced disease susceptibility 1 proteins with a lipase-like and the EP domain transduces the signal from activated NLRs downstream. This family includes EDS1, PAD4 and SAG101 that form mutually exclusive heterodimers EDS1-PAD4 and EDS1-SAG101. Despite sequence similarities, PAD4 and SAG101 control different aspects of NLR immune signaling. More specifically, PAD4 and SAG101 regulate resistance and cell death outputs of the NLR receptor pair RRS1-RPS4, respectively. Also, PAD4 and SAG101 genetically cooperate with distinct downstream signaling NLRs - ADR1 and NRG1. The main aim of this IP-LC/MS project is to assess whether PAD4 and SAG101 form complexes with ADR1 and NRG1 and to gain insight into mechanisms of the genetically established functional links between EDS1 family proteins and downstream signaling NLRs.
2021-04-06 | PXD021301 | Pride
Project description:We investigated the impacts of transition metal oxide (TMO) lithium-ion battery cathode nanomaterial, lithium cobalt oxide (LCO), on gene expression in the larvae of a model sediment invertebrate Chironomus riparius.
2020-11-08 | GSE161036 | GEO
Project description:Plants utilize cell surface-localized pattern recognition receptors (PRRs) and intracellular nucleotide-binding leucine-rich repeat (NLR) receptors to detect non-self and elicit robust immune responses. During plant development and especially during aging, fine-tuning the homeostasis of these receptors is critical to prevent their hyperactivation. Here, we show that Arabidopsis plants lacking metacaspase 1 (AtMC1) display autoimmunity dependent on immune signalling components downstream of NLR and PRR activation. Overexpression of catalytically inactive AtMC1 in an atmc1 background triggers severe autoimmunity partially dependent on the same immune signalling components. Although individual mutations in NLRs, PRRs or other immune-related components that interact with catalytically inactive AtMC1 do not rescue the autoimmune phenotype, overexpression of SNIPER1, a master regulator of NLR homeostasis, fully attenuates the phenotype, inferring that a broad defect in NLR turnover may underlie the severe autoimmunity observed. As opposed to Wt AtMC1 which exhibits a nucleocytoplasmic localization, catalytically inactive AtMC1 localizes to puncta structures that are degraded through autophagy. We infer that the phenotypes observed in plants overexpressing catalytically inactive AtMC1 may represent an additive phenotype to the relatively milder autoimmunity observed in atmc1 mutants. Altogether and considering previous evidence on the proteostatic functions of AtMC1, we speculate that Wt AtMC1 may either directly or indirectly control NLR protein levels as plants approach adulthood, thus preventing autoimmunity.
2025-03-21 | PXD048924 | Pride
Project description:Entangled photon-pair sources are at the core of quantum applications like quantum key distribution, sensing, and imaging. Operation in space-limited and adverse environments such as in satellite-based and mobile communication requires robust entanglement sources with minimal size and weight requirements. Here, we meet this challenge by realizing a cubic micrometer scale entangled photon-pair source in a 3R-stacked transition metal dichalcogenide crystal. Its crystal symmetry enables the generation of polarization-entangled Bell states without additional components and provides tunability by simple control of the pump polarization. Remarkably, generation rate and state tuning are decoupled, leading to equal generation efficiency and no loss of entanglement. Combining transition metal dichalcogenides with monolithic cavities and integrated photonic circuitry or using quasi-phasematching opens the gate towards ultrasmall and scalable quantum devices.
| S-EPMC11366010 | biostudies-literature
Project description:Given that transition metals are essential cofactors in central biological processes, misallocation of the wrong metal ion to a metalloprotein can have resounding and often detrimental effects on diverse aspects of cellular physiology. Therefore, in an attempt to characterize unique and shared responses to chemically similar metals we have reconstructed physiological behaviors of Halobacterium NRC-1, an archaeal halophile, in sub-lethal levels of Mn(II), Fe(II), Co(II), Ni(II), Cu(II) and Zn(II). Over 20% of all genes responded transiently within minutes of exposure to Fe(II), perhaps reflecting immediate large scale physiological adjustments to maintain homeostasis. At steady state, each transition metal induced growth arrest, attempts to minimize oxidative stress, toxic ion scavenging, increased protein turnover and DNA repair, and modulation of active ion transport. While several of these constitute generalized stress responses, up regulation of active efflux of Co(II), Ni(II), Cu(II), and Zn(II), down regulation of Mn(II) uptake and up regulation of Fe(II) chelation, confer resistance to the respective metals. We have synthesized all these discoveries into a unified systems level model to provide an integrated perspective of responses to six transition metals with emphasis on experimentally verified regulatory mechanisms. Finally, through comparisons across global transcriptional responses to different metals we provide insights into putative in vivo metal selectivity of metalloregulatory proteins and demonstrate that a systems approach can help rapidly unravel novel metabolic potential and regulatory programs of poorly studied organisms. Keywords: stress response, dose response
2006-05-31 | GSE4898 | GEO