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By measuring the impacts of thousands of mutations on potassium channel trafficking and function, we illuminate the molecular basis of folding, structure–function relationships, and how these are altered in disease.

Measurement of the distribution of fitness effects of new mutations arising in human oesophagus and skin, via new mathematical theory linking dn/ds values and fitness coefficients.

Linking deep mutational scanning with engineered transcriptional reporters in human cell lines establishes a generalizable method for exploring pharmacogenomics, structure, and function across broad classes of drug receptors.

Genome sequencing of mice selected for longer limbs reveals that rapid selection response is due to both discrete loci and polygenic adaptation.

The architecture of a gene regulatory network determines the effect of evolutionary changes in transcription factor binding.

Biophysical modeling, performed in silico, can predict the abundance, metabolic stability, and function of MLH1 inside living cells.

Two novel mutations in the GRIN2B gene reduce glutamate affinity by >1000-fold, reduce the receptors proton-sensitivity, and exert a dominant-negative effect over receptors in neurons.

In contrast with earlier conclusions, negative selection has a major role in cancer evolution.

Ceftriaxone resistance has arisen multiple times in clinical gonococcal populations via previously undescribed RNA polymerase mutations, underscoring the importance of continued surveillance for novel resistance determinants.

Fundamental details of the rate and molecular spectrum of transcript errors were revealed in four bacterial species, providing novel insights into transcriptional fidelity and RNA quality-control in prokaryotes.