Ontology highlight
ABSTRACT:
PROVIDER: PRJNA854614 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR19908600_1.fastq.gz | Fastqsanger.gz | |||
| SRR19908600_2.fastq.gz | Fastqsanger.gz | |||
| SRR19908601.fastq.gz | Fastqsanger.gz | |||
| SRR19908602.fastq.gz | Fastqsanger.gz | |||
| SRR19908603.fastq.gz | Fastqsanger.gz |
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Project description:In this work we took 9 samples from brain and 6 samples from muscle of the African turquoise killifish (Nothobranchius furzeri) at 3.5, 8.5 and 14 weeks. Total RNA was sequenced and circRNAs were detected.
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Project description:Aging individuals exhibit a pervasive decline in adaptive immune function, with important implications for health and lifespan. Previous studies have found a pervasive loss of immune-repertoire diversity in human peripheral blood; however, little is known about repertoire aging in other immune compartments, or in species other than humans. Here, we perform the first study of immune-repertoire aging in an emerging model of vertebrate aging, the African turquoise killifish (Nothobranchius furzeri). Despite their extremely short lifespans, these killifish exhibit complex and individualised heavy-chain repertoires, with a generative process capable of producing millions of distinct productive sequences. Whole-body killifish repertoires decline rapidly in within-individual diversity with age, while between-individual variability increases. Large, expanded B-cell clones exhibit far greater diversity loss with age than small clones, suggesting an important difference in the age-sensitivity of different B cell populations. Compared to the whole body, the immune repertoires of isolated intestinal samples exhibit much more dramatic age-related phenotypes, apparently due to an elevated prevalence of age-sensitive expanded clones. Our results highlight the importance of organ-specific dynamics in adaptive immunosenescence.
2026-03-30 | PXD029992 | Pride
Project description:Aging is associated with progressive tissue dysfunction, leading to frailty and mortality. Characterizing aging features, such as changes in gene expression and dynamics, shared across tissues or specific to each tissue, is crucial for understanding systemic and local factors contributing to the aging process. We performed RNA-sequencing on 13 tissues at 6 different ages in the African turquoise killifish, the shortest-lived vertebrate that can be raised in captivity. This comprehensive, sex-balanced 'atlas' dataset reveals the varying strength of sex-age interactions across killifish tissues and identifies age-altered biological pathways that are evolutionarily conserved. Demonstrating the utility of this resource, we discovered that the killifish head kidney exhibits a myeloid bias during aging, a phenomenon more pronounced in females than in males. In addition, we developed tissue-specific 'transcriptomic clocks' and identified biomarkers predictive of chronological age. We show the importance of sex-specific clocks for selected tissues and use the tissue clocks to evaluate a dietary intervention in the killifish. Our work provides a comprehensive resource for studying aging dynamics across tissues in the killifish, a powerful vertebrate aging model.
2026-01-04 | GSE308970 | GEO
Project description:Protein aggregation is a hallmark of age-related neurodegeneration. Yet whether aggregation drives age-related dysfunction and disease in other tissues is poorly understood. Here, we leverage the African turquoise killifish to obtain a systematic understanding of protein aggregation in seven tissues in an aging vertebrate.
2020-10-17 | MSV000086315 | MassIVE
Project description:Introduction: Aging is associated with progressive loss of renal function and vascular structure, with and without chronic kidney disease. However, the mechanisms driving renal vascular aging and potential therapeutic interventions remain poorly understood. Methods: To model this state-of-affairs, we used African turquoise killifish (Nothobranchius furzeri), a naturally short-lived vertebrate. We then inhibited the sodium-glucose co-transporter 2 inhibition (SGLT2i) to test a potential therapeutic intervention. Histological, immunofluorescent, and 3D vascular imaging were used to evaluate glomerular, tubular, and vascular changes. Single-nuclei transcriptomic profiling was performed on whole kidneys to identify age- and treatment-associated molecular signatures. Results: Aged killifish kidneys exhibited hallmark features of human renal aging, including glomerulosclerosis, tubular fibrosis, and vascular rarefaction. Functional changes included increased proteinuria and altered tubular transporter expression. Transcriptomic profiling revealed a metabolic shift from oxidative phosphorylation to glycolysis and upregulation of pro-inflammatory pathways. Aged vasculature also displayed a marked reduction in tight junctions and cell–cell contacts. Dapagliflozin attenuated age-related vascular rarefaction, preserved functional peritubular capillary networks, and reduced albuminuria by restoring a youthful transcriptional profile and enhancing intercellular signaling. However, fish lifespan was not extended. Conclusion: This study establishes the killifish as a translational model for investigating renal vascular aging. We show that SGLT2i preserves renal microvascular structure and function, reduces proteinuria, and reprograms the aged transcriptome. These results support a vascular-protective role of SGLT2i in mitigating age-related renal deterioration.
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Project description:With advancing age, senescent cells accumulate as they are not efficiently cleared by the immune system anymore. Via a senescence-associated secretory phenotype, chronic senescent cells alter the microenvironment, creating an unfavorable milieu for neurogenesis and neurorepair. Using an innovative and rapid aging model, the African turquoise killifish, we have previously demonstrated a dramatic decline in neurogenic potential of non-glial progenitors with age. Even after traumatic brain injury, progenitor proliferation and neuron production was very low in aged killifish in comparison to young adult killifish, and overall neurorepair was incomplete. In the present study, we validated if the senolytic cocktail dasatinib and quercetin (D+Q) could reboot the neurogenic output by clearing chronic senescent cells from the aged killifish brain to re-create the necessary supportive environment. Our results confirm that the aged killifish telencephalon holds a very high senescent cell burden, which we could diminish by short-term systemic D+Q treatment. As a consequence of D+Q administration, proliferation of non-glial progenitors increased and more new neurons were generated and migrated into the parenchyma after injury. Injury-induced inflammation and glial scarring, a phenomenon only seen in aged killifish, remained unaltered. Senolytic treatment with D+Q might thus hold promise for improving brain function in aged populations, and is especially interesting for reviving the neurogenic potential of an already aged central nervous system.
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Project description:Aging is a major contributor to functional decline of the heart and various cardiovascular diseases. Alterations across different cardiac cell types must be tightly orchestrated during normative aging process that has begun to be mapped at the transcriptional level through single-cell RNA-sequencing. However, current rodent models are limited in their capacity to experimentally test large numbers of candidate differentially expressed genes (DEGs). As an attractive alternative, the African Turquoise Killifish (ATK) promises more efficient genetic studies of cardiac aging because it has the shortest lifespan among vertebrates. Despite its experimental advantages, single-cell transcriptomic studies on cardiac aging in ATK have not yet been conducted. Here, we generated the first scRNA-seq profiles of hearts from young and old GRZ strain ATK and demonstrated changes in cellular composition, gene expression, functional pathways, and intercellular communication during cardiac aging.
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