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Predominant Requirement of Mitochondrial Transcriptional Factor A in Tissue-resident Regulatory T cell Maintenance and Function

ABSTRACT: Predominant Requirement of Mitochondrial Transcriptional Factor A in Tissue-resident Regulatory T cell Maintenance and Function

PROVIDER: PRJNA545234 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9141210.fastq.gz	Fastqsanger.gz
	SRR9141211.fastq.gz	Fastqsanger.gz
	SRR9141202.fastq.gz	Fastqsanger.gz
	SRR9141203.fastq.gz	Fastqsanger.gz
	SRR9141204.fastq.gz	Fastqsanger.gz

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Predominant Requirement of Mitochondrial Transcriptional Factor A in Tissue-resident Regulatory T cell Maintenance and Function

Project description:Regulatory T cells (Tregs) are pivotal for immune suppression. Cellular metabolism is important for Treg homeostasis and function. However, the exact role of mitochondrial respiration in Tregs remains elusive. Mitochondrial transcription factor A (Tfam) is essential for mitochondrial respiration and controls mitochondrial DNA replication, transcription and packaging. Here we show that genetic ablation of Tfam in Tregs impairs Treg maintenance in non-lymphoid tissues at the steady state and in tumor. Tfam-deficient Tregs have reduced proliferation and Foxp3 expression upon glucose deprivation in vitro. Tfam deficiency preferentially affects gene activation in Tregs through regulation of DNA methylation. Tfam-deficient Tregs have enhanced methylation at TSDR of Foxp3 locus. Deletion of Tfam in Tregs affects Treg homing and maintenance, resulting in tissue inflammation in colitis, but enhances tumor rejection. Thus, our work reveals a critical role for Tfam-mediated Treg respiration in regulation of inflammation and anti-tumor immunity.

2020-04-13 | GSE131883 | GEO

Requirement of Mitochondrial Transcription Factor A in Tissue-Resident Regulatory T Cell Maintenance and Function.

Project description:Regulatory T cells (Tregs) are pivotal for immune suppression. Cellular metabolism is important for Treg homeostasis and function. However, the exact role of mitochondrial respiration in Tregs remains elusive. Mitochondrial transcription factor A (Tfam) is essential for mitochondrial respiration and controls mitochondrial DNA replication, transcription, and packaging. Here, we show that genetic ablation of Tfam in Tregs impairs Treg maintenance in non-lymphoid tissues in the steady state and in tumors. Tfam-deficient Tregs have reduced proliferation and Foxp3 expression upon glucose deprivation in vitro. Tfam deficiency preferentially affects gene activation in Tregs through regulation of DNA methylation, with enhanced methylation in the TSDR of the Foxp3 locus. Deletion of Tfam in Tregs affects Treg homing and stability, resulting in tissue inflammation in colitis, but enhances tumor rejection. Thus, our work reveals a critical role of Tfam-mediated mitochondrial respiration in Tregs to regulate inflammation and anti-tumor immunity.

| S-EPMC6679941 | biostudies-literature

Heterogeneous maintenance of human tissue resident memory T cells based on efflux capacities

Project description:Tissue-resident memory T cells (TRM) accelerate pathogen clearance through rapid and enhanced functional responses in situ. In humans, TRM cells are prevalent in diverse anatomic sites throughout the human lifespan, yet mechanisms for long-term maintenance are unknown. Here, we identify subpopulations of human TRM in mucosal and lymphoid sites based on differential efflux of mitochondrial dyes, with distinct transcriptional profiles, turnover, and functional capacities. TRM are enriched in efflux(+) populations compared with circulating memory CD8+T cells. Compared to efflux- TRM, efflux(+) TRM showed transcriptional and phenotypic features of quiescence including reduced turnover, decreased expression of exhaustion markers, and increased proliferative capacity and signaling to homeostatic cytokines. Moreover, efflux(+) and efflux(-) TRM subsets both maintain TRM characteristics when activated, while efflux(+) TRM produce IL-17 and efflux(-) produce higher levels of IFN-γ and IL-2. Our results suggest a model for cooperative maintenance of T cell immunity in tissues through interplay of subsets with complementary capacities for longevity and effector function.

2018-12-26 | GSE109841 | GEO

Tfam-deficiency mediated mitochondrial disorder affects Langerhans cell maintenance and function

Project description:Langerhans cells (LCs) are skin-resident professional antigen-presenting dendritic cells (DCs) to maintain skin homeostasis. The number and function of LCs are significantly reduced during the skin aging processes, which is closely related to the aging-associated skin disorders. However, the reasons underlying the changes of LC features with age are uncertain. Mitochondria are well known to be the main powerhouse to regulate cell fitness and function, and a decline in mitochondrial quality and activity was associated with normal aging and correlated with the development of a wide range of age-related diseases. So far, it is unknown if mitochondrial abnormality is involved in skin disorders by regulating LC homeostasis. The mitochondrial transcription factor A (Tfam) acts as a nuclear-encoded transcription factor and plays a critical role in mitochondrial stabilization. To explore the role of mitochondrial quality in LC homeostasis, we generated the mice with conditional deletion of Tfam in LC lineage. We found that Tfam-deficient LCs exhibits mitochondrial abnormality including morphology and membrane permeability of mitochondria, decreased cell number as well as maturation, whereas increased phagocytosis and inflammatory response of LCs. Interestingly, age-LCs from human skin have lower Tfam expression compared to young-LCs, and have the similar features with Tfam-deficient LCs analyzed by scRNA sequence (HRA000395). Thus, our data highlight that Tfam-mediated mitochondrial stability is essential for epidermal LC maintenance and function, which might be explain the states of increased susceptible to skin infections and rising incidence of cutaneous tumor in the elder. This is the first time to investigate the effect of mitochondria abnormality on LC homeostasis, which might be helpful for therapeutic interventions in aging-associated skin pathologies.

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Project description:Increasing evidence implicates critical roles of various epitranscriptomic RNA modifications in different biological processes. Methyltransferase METTL8 installs 3-methylcytosine modification of mitochondrial tRNAs in vitro, however, its role in intact biological systems is completely unknown. Here we show that Mettl8 is localized in the mitochondria and installs m3C in mitochondrial tRNASer(UCN)/Thr in mouse embryonic cortical neural stem cells. At molecular and cellular levels, Mettl8 deletion in cortical neural stem cells leads to reduced mitochondrial protein translation and attenuated respiration activity. At the functional level, conditional Mettl8 deletion in mice results in impaired embryonic cortical neural stem cell maintenance in vivo, which can be rescued by pharmacologically enhancing mitochondrial functions. Similarly, METTL8 regulates mitochondrial protein expression and neural stem cell maintenance in human forebrain cortical organoids. Together, our study reveals a conserved epitranscriptomic mechanism of Mettl8 and mitochondrial tRNA m3C modification in maintaining embryonic cortical neural stem cells in mice and humans.

2023-01-12 | GSE214445 | GEO

in vivo CRISPR screening of ANKL-PDX targeting to iron-requirement molecules

Project description:ANKL cell proliferates predominantly in liver sinusoid depending on transferrin. However, little is known about molecular mechanism of iron-dependency of ANKL. To investigate, we performed in vivo CRISPR screening of liver resident ANKL cells targeting to genes encoding 482 iron-requirement molecules.

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Heterogeneous maintenance of human tissue resident memory T cells based on efflux capacities

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Requirement for TP73 in cancer cell maintenance and genetic alterations originating from its intragenic super-enhancer

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Tfam-deficiency mediated mitochondrial disorder affects Langerhans cell maintenance and function

Project description:Tfam-deficiency mediated mitochondrial disorder affects Langerhans cell maintenance and function

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