Non-coding mutations in microsatellite-instable (MSI) colorectal tumors are prevalent and activate cancer-specific enhancers, thereby disrupting gene expression control.

Cooperativity between two transcription regulators occurs through protein-protein interactions with a general transcription factor complex and potentiates the parallel evolution of their DNA binding sites.

Silencers and enhancers targeted by a common transcription factor in photoreceptors are distinguished by the number and diversity of binding transcription factor binding sites they contain.

Thermodynamic framework accurately predicts the sign of epistasis and its environment dependence for a canonical cis-regulatory element.

Greater phenotypic variation is exposed by mutations in a gene regulatory system compared to mutations in its constitutive components, namely the transcription factor and the promoter, alone.

A pooled mutational scanning approach for 3D chromosome conformation reveals how multiple transcription factors can jointly specify condition-specific genome conformations.

CRISPR knock-outs and functional genomic approaches probe the regulatory mechanism restricting the Hox gene Ubx to butterfly hindwings, explaining color pattern differentiation from forewings.

Mapping mutations affecting gene expression within the yeast genome and within a gene regulatory network reveals properties of the raw material for regulatory variation.

The antiviral and genomic DNA deaminase APOBEC3B is repressed in normal cells by PRC1.6/E2F6 and DREAM/E2F4 complexes and deregulation of this axis provides a unifying mechanism for overexpression in cancer.

The transcriptional control system of a sea urchin gene reveals the deep evolutionary conservation of a gene regulatory network underlying morphogenesis.