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Hannon, E. J.

Publications and source records attributed to Hannon, E. J..

2 recordsLinked to original sources

Best Practices for Pre-Processing Large-Scale ATAC-Seq Data: Why Epidemiological Studies Demand Greater Stringency

Assay for transposase accessible chromatin using sequencing (ATAC-seq) and related techniques provide critical insight into the epigenetic mechanisms that regulate gene expression in health and disease. Accurate identification of biologically meaningful chromatin accessibility signals remains an underexplored analytical challenge. Advances in sequencing technologies have increased both the magnitude and complexity of ATAC-seq datasets, leading to demand for scalable, reproducible and robust computational analysis frameworks. Peak calling, which identifies regions of chromatin accessibility, is a critical step that underpins all downstream quantitative analyses. However, there is a lack of consensus regarding the optimal peak calling strategy. Here, we present a novel bioinformatics pipeline PIPPA (Pipeline for Integrative Peak calling in Population-scale ATAC-seq), for quality control and peak set curation of large-scale ATAC-seq datasets. Using two independent cell-type sorted ATAC-seq datasets, we show that peak calling performance is dataset-dependent and that no single significance threshold performs optimally across all scenarios. We provide practical recommendations for parameters to generate high-confidence chromatin accessibility profiles. Our peak calling approach is applicable for other genome wide epigenomic assays such as ChIP-seq and CUT&Tag. By standardising this process, the PIPPA pipeline enhances epidemiological studies focused in identifying epigenetic dysregulation associated with development and disease.

bioinformatics↗

A comparison of blood and brain-derived ageing and inflammation-related DNA methylation signatures and their association with microglial burdens

Inflammation and ageing-related DNA methylation patterns in the blood have been linked to a variety of morbidities, including cognitive decline and neurodegenerative disease. However, it is unclear how these blood-based patterns relate to patterns within the brain, and how each associates with central cellular profiles. In this study, we profiled DNA methylation in both the blood and in five post-mortem brain regions (BA17, BA20/21, BA24, BA46 and hippocampus) in 14 individuals from the Lothian Birth Cohort 1936. Microglial burdens were additionally quantified in the same brain regions. DNA methylation signatures of five epigenetic ageing biomarkers ( epigenetic clocks), and two inflammatory biomarkers (DNA methylation proxies for C-reactive protein and interleukin-6) were compared across tissues and regions. Divergent correlations between the inflammation and ageing signatures in the blood and brain were identified, depending on region assessed. Four out of the five assessed epigenetic age acceleration measures were found to be highest in the hippocampus ({beta} range=0.83-1.14, p[≤]0.02). The inflammation-related DNA methylation signatures showed no clear variation across brain regions. Reactive microglial burdens were found to be highest in the hippocampus ({beta}=1.32, p=5x10-4); however, the only association identified between the blood- and brain-based methylation signatures and microglia was a significant positive association with acceleration of one epigenetic clock (termed DNAm PhenoAge) averaged over all five brain regions ({beta}=0.40, p=0.002). This work highlights a potential vulnerability of the hippocampus to epigenetic ageing and provides preliminary evidence of a relationship between DNA methylation signatures in the brain and differences in microglial burdens.

neuroscience↗