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SMRT controlled inflammation in cDC1 is orchestrated through mTOR-Succinate axis despite of suppressed glycolysis

ABSTRACT: SMRT controlled inflammation in cDC1 is orchestrated through mTOR-Succinate axis despite of suppressed glycolysis

PROVIDER: PRJEB67355 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR12110336_1.fastq.gz	Fastqsanger.gz
	ERR12110336_2.fastq.gz	Fastqsanger.gz
	ERR12110337_1.fastq.gz	Fastqsanger.gz
	ERR12110337_2.fastq.gz	Fastqsanger.gz
	ERR12110338_1.fastq.gz	Fastqsanger.gz

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SMRT controlled inflammation in cDC1 is orchestrated through mTOR-Succinate axis despite of suppressed glycolysis

Project description:Immunogenic activation of DCs by TLRs involves coordinated metabolic and transcriptional rewiring. The negative regulation of such metabolic rearrangements in DCs remains elusive. We have recently reported that Ncor2 (SMRT) loss of function renders cDC1 DCs to be highly inflammatory in nature by polarizing the naïve CD4+T cells towards the Th1 phenotype. Here, we sought to establish an immunometabolic relationship, underlying its phenomena. We performed high throughput transcriptional and metabolic analysis and identified SMRT ablated DCs to have enhanced OXPHOS but reduced glycolysis, de novo FAS, and β-oxidation upon TLR9-specific activation. Mechanistically, decreased mTOR expression favoured the reduced glycolytic rate and its induction with Mhy1485 lowered the secretory levels of inflammatory cytokines. Additionally, decreased Pdh expression and subdued acetyl-CoA levels gave an insight into the broken TCA cycle. Correspondingly, they were found to rewire the cycle by activating the anaplerotic glutamine catabolism and succinate oxidation to maintain the inflammatory status of the cell. Inhibition of succinate transport with DEBM in sync with mTOR induction drastically hampered the inflammatory response both at RNA and protein levels. To validate the same at the global mRNA level we did bulk RNA-seq to determine the differentially expressed genes in different experimental settings. The results thus obtained showed transcriptional dysregulation of inflammatory pathways in SMRT KD DCs with combined modulator treatment.

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RNA-seq of Zbtb10 Knockdown and Control cDC1 dendritic cells (Cd8+)

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Project description:To identify the direct targets of Zeb1 we performed ChIP-seq of wild type cDC1 cell line in unstimulated condition. cDC1 cell line was used for Chromatin Immunoprecipitation, it was then fixed and crosslinked and then fragmented and the fragmented DNA-protein was immunoprecipated using Zeb1 antibody. The chromatin sample was then used to prepare library using NEB kit following the manufacturer's protocol

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Succinate dehydrogenase deficiency-driven succinate accumulation induces drug resistance in acute myeloid leukemia via ubiquitin-cullin regulation

Project description:Drug resistance is vital for the poor prognosis of acute myeloid leukemia (AML) patients, but the underlying mechanism remains poorly understood. Given the unique microenvironment of bone marrow, we reasoned that drug resistance of AML might rely on distinct microenvironment-associated metabolic processes. Here, we identified SDH deficiency and over-cumulative succinate as typical features in AML, with a marked function in causing the resistance of AML cells to a wide range of anti-cancer therapies. Mechanistically, succinate promoted the accumulation of oncogenic proteins in a manner that precedes transcriptional activation. This function was mediated by succinate-triggered upregulation of UBC12 phosphorylation, which impaired its E2 function in cullins neddylation. Notably, decreasing succinate levels by fludarabine could effectively restore the drug sensitivity of SDH-deficient AML PDX. Together, we uncover a novel function of succinate in driving drug resistance by regulating p-UBC12/cullin activity, and indicate reshaping succinate metabolism as a promising treatment for SDH-deficient AML.

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Monocarboxylate transporters facilitate succinate uptake into brown adipocytes

Project description:Uptake of circulating succinate by brown adipose tissue (BAT) and beige fat elevates whole-body energy expenditure, counteracts obesity, and antagonizes systemic tissue inflammation in mice. The plasma membrane transporters that facilitate succinate uptake in these adipocytes remain undefined. Here we elucidate a mechanism underlying succinate import into BAT via monocarboxylate transporters (MCTs). We show that succinate transport is strongly dependent on the proportion of it present in the monocarboxylate form. MCTs facilitate monocarboxylate succinate uptake, which is promoted by alkalinization of the cytosol driven by adrenoreceptor stimulation. In brown adipocytes, we show that MCT1 primarily facilitates succinate import. In mice, we show that both acute pharmacological inhibition of MCT1 and congenital depletion of MCT1, decrease succinate uptake into BAT and consequent catabolism. In sum, we define a mechanism of succinate uptake in BAT that underlies its protective activity in mouse models of metabolic disease.

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