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Barlow, J. P.

Publications and source records attributed to Barlow, J. P..

2 recordsLinked to original sources

Translational toolkit for reproducible, cross-study profiling of human ageing hallmarks in human blood and tissue

BackgroundAgeing is a complex, multi-dimensional process, underpinned by interacting biological hallmarks that collectively contribute to functional decline and increased susceptibility to disease. While considerable progress has been made in delineating individual ageing pathways, translation into human studies has been hindered by methodological heterogeneity and a lack of standardised, multi-system approaches. Here, we describe a validated, high-resolution toolkit for the simultaneous quantification of multiple ageing hallmarks in clinically accessible human samples, encompassing cellular senescence, immune ageing, inflammation, mitochondrial function, mTOR signalling, autophagy, genomic instability, and stem cell exhaustion. MethodsBlood (25ml) was obtained from young and aged donors (26-81y). Deep immunophenotyping was performed using a novel 30-colour spectral flow cytometry panel. T-cell mTOR activation and autophagic flux were assessed by flow cytometry. Metabolic flux was measured by Seahorse. From whole blood (4 ml), muscle, and adipose tissue (AT) (obtained during elective hip arthroplasty) RNA, DNA, AT stem cells, and myoblasts were isolated. DNA copy number and senescent cell burden were assessed by q-PCR and SA-{beta}-gal staining, respectively. FindingsUtilising this toolkit, we identified pronounced age-related immune remodelling, increased senescent T-cell burden, diminished mitochondrial capacity and altered mTOR-autophagy signalling between healthy young and aged donors. Furthermore, metabolism was significantly affected by anti-coagulant and freezing sample before analysis. InterpretationThis integrated platform provides a foundation for reproducible, cross-study analyses and facilitates translational investigation of interventions targeting health-span extension. FundingWellcome Leap Dynamic Resilience program (co-funded by Temasek Trust).

immunology↗

UPF1 is required for gene expression in mitochondria and for the elimination of paternal mtDNA

UPF1 is a conserved RNA helicase in eukaryotes typically defined by its role in nonsense-mediated mRNA decay (NMD). This study presents ChIP-seq evidence indicating an RNA-dependent interaction of UPF1 with mtDNA, consistent with an RNA-mediated association. Mitochondrial localisation was observed as discrete foci throughout the mitochondrial network, frequently in proximity to nucleoids, as confirmed microscopically by immunostaining and GFP tagging of UPF1 in different fly tissues and S2 cells. Depletion of UPF1, but not depletion of the other core NMD factors UPF2 or UPF3, in salivary glands results in smaller mitochondria and, unexpectedly, increased respiratory activity. This increase is observed specifically in salivary glands and correlates with elevated expression of nuclear genes involved in respiratory chain assembly and mitochondrial translation. Changes in mtDNA-encoded gene expression are also observed upon the depletion of UPF1. These findings indicate that UPF1 operates in mitochondria and, independently of canonical NMD, is linked to mitochondrial gene expression and may coordinate nuclear and mitochondrial gene expression in a tissue-specific manner.

cell biology↗