Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
Cells resembling human fetal adrenal neuroblasts have been identified as major neuroblastoma cancer cells through single-cell mRNA comparison. Tumor risk stratification correlates with the differentiation of neuroblast-like neuroblastoma cells.
Case–case genome-wide association studies (GWAS) within a single genotyped cohort have proven useful in identifying genetic variants explaining different health outcomes, yet they are limited by data availability. A new study by Peyrot and Price proposes a clever statistical method to overcome this problem by inferring case–case GWAS results from a pair of standard case–control GWAS summary statistics that need not be from the same cohort.
Polycomb-group proteins assemble into two primary complexes—Polycomb repressive complex (PRC) 1 and 2—that safeguard cell fate by repressing gene transcription. Two new studies explore the PRC1 landscape during the transition from gametes to embryos in mice, thus providing insight into the intergenerational transmission of epigenetic information and gene regulation dynamics as embryos prepare for gastrulation.
The structure of chromatin is associated with its function, but precisely how is unclear. New data show that the higher-order architecture of the genome is similar among cell types with widely variant fates and gene expression patterns, thus challenging the view that chromatin domains determine function in the genome.
Stretches of non-coding DNA that have remained identical across millions of years of evolution are typically assumed to have functional regulatory roles that would be compromised by any amount of nucleotide substitution. A new study finds that these ultraconserved regions are more robust to mutagenesis than their level of conservation would suggest.
Immune responses require a delicate balance: a weak response can cause immunodeficiency, whereas an excessive response can lead to hyperinflammatory disease and hematological malignancy. Because spleen tyrosine kinase has roles in multiple signaling pathways, its gain-of-function alterations in humans cause hypogammaglobulinemia as well as autoinflammation and predisposition to B cell lymphoma.
A new study builds a novel deep-learning approach to unravel the syntax of transcription-factor binding from high-resolution ChIP–nexus data. In silico simulations lead to experimental validation of complex sequence-based predictions: helical periodicity and directional cooperativity between transcription factors.
Chromosomal inversions frequently underlie distinct phenotypic variation. A new study shows that in butterflies, inversion haplotypes accumulate deleterious mutations that prevent fixation in natural populations.
Chromatin structure, specifically sites of open or accessible chromatin, regulates transcription-factor binding, thereby determining cell-type-specific gene expression. Two new studies identify a constant requirement for SWI/SNF-complex remodeling to maintain open chromatin. In both studies, acute inhibition or degradation of the BRG1 or BRM ATPase subunits through chemical or genetic methods led to a loss of chromatin accessibility, in some cases affecting transcription-factor binding and altered gene expression.
Half of all colorectal cancers bear KRAS-activating mutations that affect the metabolic dependencies of cancer cells and drive resistance to commonly used drugs. A new study provides insights into KRAS-driven metabolic rewiring and identifies a new therapeutic target for KRAS-mutant cancers.
