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PolyGembler, a method for grouping and ordering contigs into complete pseudomolecules by combining long-read sequencing and genotype information from an outbred mapping population, improves the accuracy for assembly of polyploidy plant genomes.
Single-cell RNA-seq of a collection of 200 cancer cell lines finds common, recurrent heterogeneous expression programs, which also are found in patient samples and are linked to cell state and drug sensitivity.
This Perspective explores the concept of tumor promotion and shows how carcinogenesis experiments performed decades ago in mice are remodeling the view of cancer initiation and prevention.
Environmental exposures shape patterns of selection for mutations in clonal hematopoiesis. Cancer therapies promote the growth of clones with mutations that are strongly enriched in treatment-related myeloid neoplasms.
Whole-genome sequencing of wheat populations from 25 subspecies within the genera Triticum and Aegilops provides insights into the role of evolutionary constraints in shaping the adaptive landscape of bread wheat.
Single-cell chromatin profiling of different brain regions identifies cell-type-specific regulatory elements, and helps to predict functional SNPs for Alzheimer’s and Parkinson’s diseases.
CHESS is an algorithm that compares chromatin contact maps and identifies differential features. It can analyze interspecies syntenic regions and three-dimensional changes caused by genetic perturbation.
dACE2 is a newly identified isoform of ACE2 that is unable to bind the SARS-CoV-2 spike protein. Truncated dACE2, but not full-length ACE2, is induced by interferons and viruses, thus suggesting that such conditions are unlikely to increase cellular entry of SARS-CoV-2.
A truncated angiotensin-converting enzyme 2 (ACE2) isoform that lacks domains required for severe acute respiratory syndrome coronavirus 2 binding exhibits tissue-specific expression patterns and is responsive to interferon stimulation, in contrast to full-length ACE2, which is unresponsive to interferons.
Super-resolution microscopy identifies sub-topologically associating domain (TAD) nanodomains and intercellular heterogeneity in TAD conformation and insulation. Cohesin or CTCF depletion regulates distinct types of chromatin contacts at the TAD but not nanodomain level.
Analysis of two independent cohorts of patients with Bardet–Biedl syndrome (BBS) with known recessive biallelic pathogenic mutations in one of 17 BBS genes shows an enrichment of rare nonsynonymous secondary variants in the same gene set, with significant over-representation of secondary alleles in chaperonin-encoding genes.
Genome-wide association analyses in the Japanese population and trans-ancestry meta-analyses identify new risk loci for coronary artery disease. A polygenic risk score derived from these findings identifies individuals with increased risk of long-term cardiovascular mortality.
Somatic mutational loads in cancer genomes change with chromatin domain boundaries. Different mutational processes lead to distinct somatic mutation distributions in active versus inactive domains, including during tumor evolution.
MR-JTI, a unified framework for joint-tissue imputation and Mendelian randomization, improves prediction performance in a tissue-dependent manner when applied to large-scale biobanks and meta-analysis data.
High-throughput chromosome conformation enhancer capture identifies dynamic enhancer networks that regulate differentiation of human mesenchymal stem cells. Transcription factors (TFs) at baited enhancers appear to stabilize TF binding at target enhancers.
Genetic tools can help uncover evolutionary histories, migration patterns and admixture events of domesticated animals and their wild ancestors. The genetic window into the past can help shape breeding strategies and inform animal agricultural practices that should lead to a more resilient and sustainable future.
FOXA1 is a key pioneer factor in androgen-receptor activity but has been an elusive drug target. A new study shows that inhibition of the associated cofactor LSD1 modifies the methylation state of FOXA1, thus resulting in chromatin dissociation and tumor inhibition, even in models of treatment-resistant prostate cancer.