Weak yet highly species-specific protein-protein interactions enhance the activity of metabolically related enzymes in bacteria at endogenous conditions, but also mean that overexpression of one partner leads to permanent non-physiological complexes and gene dosage toxicity.

Multiple replicated examples of epistasis affecting gene expression in humans are identified, some explaining a substantial proportion of the variation in expression.

A combination of window-of-sensitivity, genetic, and in vitro findings illuminate mechanisms of gene–environment interaction in a multifactorial model of a common birth defect.

Calcium channel blockers accelerate aortic aneurysm and cause premature aortic rupture in a mouse model of Marfan syndrome through protein kinase C-mediated activation of extracellular signal-regulated kinase.

The Polycomb group protein SCML2 contributes to the assembly and gene silencing function of Polycomb Repressive Complex 1 (PRC1) and requires an RNA-binding region to reach chromatin targets.

A post-translational modification called O-GlcNAcylation modulates the activity of the SOX2 transcription factor in pluripotent stem cells.

A small molecule called Sm4 can disrupt interactions involving a transcription factor called Sox18, while having little impact on other members of the SoxF family.

Tailoring instructive experience to individual genetic biases improves vocal learning outcomes across genetic backgrounds in the Bengalese finch.

Regulatory evolution allows paralogs to escape from strucural pleiotropy.

Analysis of data on drug-gene interactions suggests that decentralized collaboration will increase the robustness of scientific findings in biomedical research.