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Regulation of intracellular pH by SLC4A7 tunes mTORC1 function to promote plasma cell differentiation

ABSTRACT: Regulation of intracellular pH by SLC4A7 tunes mTORC1 function to promote plasma cell differentiation

PROVIDER: PRJNA1122164 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29350231_1.fastq.gz	Fastqsanger.gz
	SRR29350231_2.fastq.gz	Fastqsanger.gz
	SRR29350232_1.fastq.gz	Fastqsanger.gz
	SRR29350232_2.fastq.gz	Fastqsanger.gz
	SRR29350233_1.fastq.gz	Fastqsanger.gz

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Regulation of intracellular pH by SLC4A7 tunes mTORC1 function to promote plasma cell differentiation

Project description:B cells differentiate into antibody-producing plasma cells, which are critical for humoral immunity, autoimmunity, and vaccine responses. Despite the importance of environmental stressors on regulating humoral immune responses, the influence of pH on PC differentiation has not been described. Here, we identified SLC4A7, a sodium/bicarbonate cotransporter, as a selective regulator of PC differentiation. SLC4A7 deletion impaired the formation of PCs and humoral immunity to influenza A virus infection in mice. Mechanistically, we find that SLC4A7 prevents acidification of intracellular pH and thus maintains lysosomal function and mTORC1 activity. Loss of SLC4A7 suppresses PC differentiation under conditions of extracellular acidosis in vitro and in a mouse model of metabolic acidosis. Here we reveal a novel relationship between the regulation of intracellular pH by SLC4A7 and mTORC1-dependent PC differentiation and humoral immunity.

2024-06-14 | GSE269509 | GEO

Histone acetylation regulates intracellular pH

Project description:Differences in global levels of histone acetylation occur in normal and cancer cells, although the reason cells regulate these levels has remained unclear. Here we demonstrate a role for histone acetylation in regulating intracellular pH (pHi). As pHi decreases, histones are globally deacetylated by histone deacetylases (HDACs) and the released acetate anions are co-exported with protons out of the cell by monocarboxylate transporters (MCTs), preventing further reductions in pHi. Conversely, global histone acetylation increases at more alkaline pHi, such as when resting cells are induced to proliferate. Inhibition of HDACs or MCTs decreases acetate export and lowers pHi, particularly compromising pHi maintenance in acidic environments. Global deacetylation at low pH is reflected at a genomic level by decreased abundance and extensive redistribution of acetylation at promoters and intergenic regions. Thus acetylation of chromatin functions as a rheostat to regulate pHi with important implications for therapeutic use of HDAC inhibitors. To investigate the redistribution of H4K16ac throughout the genome upon treatment at pH 6.5

2012-11-04 | E-GEOD-40114 | biostudies-arrayexpress

Histone acetylation regulates intracellular pH

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Acidity perturbs IL-2 responsiveness, mTORC1 and c-Myc in CD8+ T cells

Project description:CD8+T cells play a critical role in tumor control but a range of barriers in the microenvironment including low pH can suppress their function.Here, we demonstrate that acidity dampens T-cell expansion mainly due to impaired IL-2 responsiveness, blunts cytokine secretion upon re-activation, and lowers the cytolytic capacity ofCD8+T cells expressing weak affinity TCR. We further reveal decreases in both mTORC1 signaling and c-Myc levels at low pH.Mechanistically, concomitantly to nuclear/cytoplasmic acidification, mTORC1 was disrupted in a Rheb-, Akt/TSC2/PRAS40-, GATOR1- and Lkb1/AMPK -independent manner, and c-Myc levels dropped due to both decreased transcription and higher proteasome-mediated degradation. In addition, lower intracellular levels of glutamine/glutamate/aspartate and elevated proline were observed with no apparent impact on mTORC1 or c-Myc. Overall, we conclude that, due to the broad disruption caused by acidity, multiple interventions will be required to restore T-cell function unless intracellular pH can be effectively restored.

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An environmental code tunes the intracellular signaling network activity to shape cellular responses

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Measuring the dependence of the yeast heat shock response on intracellular pH and translation during stress

Project description:S. cerevisiae cells acidify when they experience stressful temperatures. In addition, newly-translated proteins are thought to misfold, triggering the heat shock response. To determine whether heat-shock associated acidification and translation state are important for the cellular response, we manipulated intracellular pH, blocked translation, heat shocked cells, and sequenced the transcriptome.

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Project description:Galectin-3 is a carbohydrate binding protein implicated in cell-cell interaction and cell growth. Interestingly, recent studies suggest that galectin-3 is involved in cell metabolism and linked to diabetes and cancer. How galectin-3 might act as a diabetogenic and tumorogenic factor remains to be investigated. Here we report that intracellular galectin-3 is physically associated with Rag GTPases and Ragulator of the mTORC1 signaling machinery on lysosomes. We show that galectin-3 senses lipopolysaccharide (LPS) to facilitate the interaction of Rag GTPases and Ragulator, leading to activation of Rag GTPases thus lysosomal loading of mTOR and activation of mTORC1. Integrative genomics and transcriptomics analyses reveal that the LPS/galectin-3-Rag GTPases/Ragulator-mTORC1 axis regulates a cohort of genes including GLUT1 (glucose transporter member 1) that functions in glucose uptake and glycolysis and HK2 (hexokinase 2) and PKM2 (pyruvate kinase M2) that catalyze the first and last step of glycolysis, respectively. Indeed, galectin-3 deficiency severely compromises LPS-promoted glycolysis. Importantly, in diabetes patients, the expression of HK2 was significantly reduced, and in hepatocellular carcinoma (HCC), thyroid cancer, and prostate cancer, galectin-3 is highly expressed, and its level of expression is positively correlated with that of HK2 and PKM2 and negatively correlated with the prognosis of HCC patients. Our study unravels that galectin-3 is a sensor of LPS, an important modulator of the mTORC1 signaling, and a critical regulator of glucose metabolism, adding to the understanding of diabetogenesis and tumorigenesis.

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