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Genome-wide CRISPR screening identifies thymidine nucleotide metabolism as a key regulator of human telomere length. Thymidine supplementation promotes telomere elongation in cells derived from patients with telomere biology disorders.
Genetic lineage tracing in mice shows that endocardium-derived fibroblasts preferentially proliferate in response to pressure overload. Ablation of these cells alleviates cardiac fibrosis and reduces functional decline after pressure overload injury.
Adjusting for common variant polygenic scores improves yield in gene-based rare variant association tests for quantitative traits, particularly when using sparse mixed models or simple linear models as an alternative to dense mixed-model approaches.
Quantifying whether different populations share similar effect sizes of common causal variants is vital to understand the genetic basis of disease and build better prediction models. A new study proposes a method leveraging admixture to estimate the correlation of causal genetic variants and finds they are largely similar across ancestry backgrounds.
This analysis of individuals of admixed genetic ancestries suggests that complex trait causal variant effect sizes are, by and large, similar across ancestries, and discusses the implications for the study of these and other diverse populations.
We introduce molecular and cellular criteria — based on morphology, ploidy, CpG island methylation and immune infiltration — that improve the characterization of malignant pleural mesothelioma. These criteria reveal adaptation strategies that are adopted by tumor cells and offer new possibilities for classification and clinical management.
Meta-analyses of genome-wide association studies for endometriosis identify 49 distinct association signals. Fine-mapping of causal variants explores functional effects across various tissues. Genetic correlations between endometriosis and other pain conditions are also highlighted.
Multi-ancestry genome-wide association analyses and systematic variant-to-gene mapping strategies implicate new genes and pathways influencing lung function and chronic obstructive pulmonary disease risk.
Transitional liver progenitor cells (TLPCs), which derive from biliary epithelial cells (BECs), differentiate into hepatocytes after serious liver damage. Notch and WNT/β-catenin signaling regulate BEC-to-TLPC and TLPC-to-hepatocyte conversions, respectively.
Premalignant stromal cells from women with germline BRCA1 mutations exhibit increased expression of secreted factors regulating epithelial homeostasis in a paracrine fashion. These secreted factors, such as MMP3, promote premalignant epithelial changes including elevated proliferation and altered differentiation of a subpopulation of luminal progenitor cells.
