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Telomere length is an important determinant of cellular aging and disease risk, but the genetics of telomere length control in humans is unclear. A genome-wide CRISPR screen has now identified a central role for thymidine nucleotide metabolism in the regulation of telomere length, which has implications for the diagnosis and treatment of disease.
A new study deciphers the origin and evolution of childhood neuroblastoma using genome sequencing data, mathematical models and statistical inference, showing how neuroblastoma evolution is an accurate predictor of outcome.
How histone modifications are reprogrammed through germline development in plants is poorly understood. We found that H3K27me3 and H3K4me3 are extensively reprogrammed throughout the development of Arabidopsis male gametophyte. This reprogramming leads to widespread chromatin bivalency and selective removal of H3K27me3 marks from key developmental regulators in sperm.
Analysis of multiple tumor types, cancer cell lines and adult tissues identifies tumor-specific transposable-element-chimeric transcripts. Mass spectrometry data confirm that many are translated and subsequently located on the extracellular surface of cancer cells, highlighting potential immunogenic therapies.
Somatic evolutionary analysis of neuroblastoma, a pediatric tumor, proposes a common fetal time of origin. Notably, high-risk tumors exhibit early genomic instability and prolonged evolution, and this evolutionary duration predicts clinical outcomes.
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.
