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MLA

ABSTRACT: MLA

PROVIDER: PRJEB64869 | ENA |

REPOSITORIES: ENA

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Dataset's files

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			Action	DRS
	ERR11856300_1.fastq.gz	Fastqsanger.gz
	ERR11856300_2.fastq.gz	Fastqsanger.gz
	ERR11857300_1.fastq.gz	Fastqsanger.gz
	ERR11857300_2.fastq.gz	Fastqsanger.gz
	ERR11857400_1.fastq.gz	Fastqsanger.gz

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Meningeal lymphatic ablation reduces ischemic stroke-induced inflammation via reprograming transcriptome profiling in cervical lymph nodes [RNA-seq]

Project description:Meningeal lymphatic system governs immune cell trafficking in the brain via brain-to-cervical lymph node (CLN) pathway. However, the role of meningeal lymphatics in brain–CLN axis after stroke remains unclear. Here, we showed that meningeal lymphatic ablation (MLA) reduced brain infarct and neuronal loss levels and inhibited inflammatory pathways in the hippocampus after MCAO–reperfusion. Single-cell transcriptome analysis demonstrated that MLA reduced monocyte/macrophage and polymorphonuclear cell counts and T and natural killer cell effector function. MLA reprogrammed the transcriptome profile related to chemotaxis and leukocyte migration in CLN LECs and downregulated expression of the CCN1 in floor LECs. Mechanistically, MLA inhibited inflammatory macrophage infiltration by repressing CCN1 and CD147 (thromboinflammatory marker) expression in blood vessels, thus inhibiting detrimental inflammatory responses. Blockade of VEGF-C-mediated signaling in meningeal lymphatic system improved memory function after ischemic stroke. Collectively, MLA reprograms the LEC transcriptome and inhibits CCN1-mediated proinflammatory responses during poststroke brain–CLN signaling.

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Meningeal lymphatic ablation reduces ischemic stroke-induced inflammation via reprograming transcriptome profiling in cervical lymph nodes [scRNA-seq]

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Time course RNA-seq analysis of expression changes upon MLACC expression in Arabidopsis using a dexamethasone-inducible system which mirrors NLR activation

Project description:Innate immune responses of plant cells confer the first line of defence against pathogens. Signals generated by activated receptors are integrated inside the cell and converge on transcriptional programmes in the nucleus. The barley NLR intracellular receptor MLA is fully functionnal in Arabidopsis and the MLA N-terminal coiled-coil domain (MLACC) is sufficient for initiating the MLA-dependent immune signalling. Using RNA-seq, we analyzed the early MLACC-mediated transcriptional changes over time in a dexamethasone-inducible and pathogen-independent system.

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Project description:Disease resistance is mediated by specific recognition of pathogen avriulence effectors (AVR) by nucleotide-binding leucine-rich repeat (NLR) receptors. The barley (Hordeum vulgare) mildew locus A (mla) resistance gene homolog 1 (RGH1) encoded NLRs (MLAs) confer isolate-specific resistance to the widespread mildew fungus Blumeria graminis forma specialis hordei (Bgh). In barley, MLA has been subject to extensive functional diversification, resulting in allelic resistance specificities, each recognizing a cognate Bgh AVRa. The by genetic association isolated AVRa1 and AVRa13 effectors belong to the candidate secreted effector protein (CSEP) gene family (Lu et al., 2016). To unravel the complex mechanisms underlying MLA functional diversification in barley and wheat, isolation of numerous Bgh AVRa genes and recognition of their gene products by MLA is necessary. Our here deployed higher resolution genetic association approach identified the Bgh avirulence gene candidate loci AVRa7, AVRa9, AVRa22 and AVRa10 by associating of transcript polymorphisms and AVRa phenotypes from a collection of 27 Bgh isolates. We collected 10 Bgh isolates from a local Bgh population in Cologne in addition to our previous collection of 17 Bgh isolates (Lu et al., 2016).

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