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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.
