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A Virus-acquired Host Cytokine Controls Systemic Aging by Antagonizing Apoptosis

ABSTRACT: A Virus-acquired Host Cytokine Controls Systemic Aging by Antagonizing Apoptosis

PROVIDER: PRJNA436344 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6792080.fastq.gz	Fastqsanger.gz
	SRR6792081.fastq.gz	Fastqsanger.gz
	SRR6792074.fastq.gz	Fastqsanger.gz
	SRR6792075.fastq.gz	Fastqsanger.gz
	SRR6792076.fastq.gz	Fastqsanger.gz

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A Virus-acquired Host Cytokine Controls Systemic Aging by Antagonizing Apoptosis

Project description:Aging is characterized by degeneration of unique tissues. However, dissecting the interconnectedness of tissue aging remains a challenge. Here, we employ a muscle-specific DNA damage model in Drosophila to reveal secreted factors that influence systemic aging in distal tissues. Utilizing this model, we uncovered a cytokine, Diedel, that when secreted from muscle or adipose can attenuate age-related intestinal tissue degeneration by promoting proliferative homeostasis of stem cells. Diedel is both necessary and sufficient to limit tissue degeneration and extend lifespan. Secreted homologs of Diedel are also found in viruses, having been acquired from host genomes. Focusing on potential mechanistic overlap between cellular aging and viral-host cell interactions and, we found that Diedel is a functionally conserved inhibitor of apoptosis and can act as a systemic rheostat to modulate cell death during aging. These results highlight a key role for secreted antagonists of apoptosis in the systemic coordination of tissue aging.

2018-07-02 | GSE111248 | GEO

A virus-acquired host cytokine controls systemic aging by antagonizing apoptosis.

Project description:Aging is characterized by degeneration of unique tissues. However, dissecting the interconnectedness of tissue aging remains a challenge. Here, we employ a muscle-specific DNA damage model in Drosophila to reveal secreted factors that influence systemic aging in distal tissues. Utilizing this model, we uncovered a cytokine-Diedel-that, when secreted from muscle or adipose, can attenuate age-related intestinal tissue degeneration by promoting proliferative homeostasis of stem cells. Diedel is both necessary and sufficient to limit tissue degeneration and regulate lifespan. Secreted homologs of Diedel are also found in viruses, having been acquired from host genomes. Focusing on potential mechanistic overlap between cellular aging and viral-host cell interactions, we found that Diedel is an inhibitor of apoptosis and can act as a systemic rheostat to modulate cell death during aging. These results highlight a key role for secreted antagonists of apoptosis in the systemic coordination of tissue aging.

| S-EPMC6072105 | biostudies-literature

SLEAR predisposes to systemic lupus erythematosus by regulating apoptosis

Project description:SLEAR predisposes to systemic lupus erythematosus by regulating apoptosis

| PRJNA412809 | ENA

Extracellular pyridine nucleotides mediate systemic acquired resistance in Arabidopsis thaliana

Project description:Systemic acquired resistance (SAR) is a long-lasting broad-spectrum plant defense mechanism that is induced by mobile signals generated in the primarily infected leaves. Although multiple mobile SAR signals have been proposed, how these signals are perceived in the systemic leaves is unknown. Here, we show that extracellular nicotinamide adenine dinucleotide (phosphate) (eNAD(P)) accumulates in the systemic leaves and that both eNAD(P) and its receptor, the lectin receptor kinase (LecRK), LecRK-VI.2, are required in the systemic leaves for the establishment of SAR. Moreover, the mobile signal N-hydroxypipecolic acid (NHP) induces de novo NAD(P) leakage in the systemic leaves through the respiratory burst oxidase homolog RBOHF-produced reactive oxygen species (ROS). Importantly, NHP-induced systemic immunity depends on ROS, eNAD(P), and the eNAD(P) receptor complex LecRK-VI.2/ BAK1, indicating that NHP triggers SAR through the ROS-eNAD(P)-LecRK-VI.2/BAK1 signaling pathway. Our results uncovered a long-sought-after mechanism underlying the perception of mobile SAR signals in the systemic leaves

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Extracellular pyridine nucleotides mediate systemic acquired resistance in Arabidopsis thaliana

Project description:Extracellular pyridine nucleotides mediate systemic acquired resistance in Arabidopsis thaliana

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RNA-seq experiment to investigate the effect of inactivating the Apoptosis Antagonizing Transcription Factor (Aatf)

Project description:Human nephronophthisis and related ciliopathies suggest a link between ciliary signaling defects and altered DNA damage responses. The goal of our study is to elucidate the molecular link of both signaling systems as well as the role of altered DNA damage responses in kidney degeneration and fibrosis. The kinase-regulated DNA damage response target Apoptosis Antagonizing Transcription Factor (Aatf) is a master regulator of the p53 response. Upon genetic deletion of Aatf in renal tubular cells we induce progressive renal failure and a phenotype closely resembling human nephronophthisis in mice and are able to show Aatf as a regulator of primary cilia and modulator of the DNA damage response connecting two pathogenetic concepts of nephronophthisis and nephronophthisis-related ciliopathies. The analysis of the RNA-sequencing of four Aatf-knockout mice and four wildtype mice supports the experimental findings.

2019-03-31 | E-MTAB-7077 | biostudies-arrayexpress

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Increased Apoptosis and aberrant apoptosis signaling pathways of CD4+CD25+FOXP3+ regulatory T cells in patients with systemic lupus erythematosus

Project description:Background: Systemic Lupus Erythematosus (SLE) is a prototype of autoimmune disease. Decreased cell numbers and suppressive defects of naturally occurring CD4+CD25+FOXP3+ regulatory T cells (Tregs) play an important role in the breakdown of SLE immune tolenrance. We have peviously observed significantly increased apoptosis of peripheral blood CD4+ T cells in SLE patients. Our objective here was to detect the apoptosis of Tregs in SLE patients to see if it could contribute to reduced suppressive activity of Tregs, and further elucidate the genes and signaling pathways which trigger the apoptosis in these cells. Methods and findings: The cell number and apoptosis rates of Tregs was respectively evaluated in SLE patients and normal controls (NCs) by FACS. The suppressive activity of Tregs was measured by coculture with CD4+CD25-CD127dim/- T cells. The relationship of abnormal Tregs apoptosis with clinical parameters was analyzed by Pearson correlation analysis. Gene expression profiles of unstimulated Tregs from active SLE patients and NCs were generated by microarray analysis. Differential genes expression was verified by real time-PCR. We found that the Tregs from SLE patients showed a significantly reduced number, elevated apoptosis rates and impared suppressive capacity compared to NCs. The increased apoptosis of Tregs was negatively correlated with the total number of Tregs and positively correlated with disease activities. Gene expression profiles of unstimulated Tregs from recent-onset SLE subjects reveal a cellular response that could make the cells sensitive to apoptosis, partially due to the stress responses, DNA-damaging and cytokine stimulation. This global picture of pathway-specific expression signatures is a step further into dissecting Tregs defects in the pathogenesis of SLE.

2023-04-03 | GSE154552 | GEO

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