In its capacity to switch into a heritable, prionogenic form, a conserved RNA-modifying enzyme epigenetically alters fundamental growth, aging, and protein synthesis properties of eukaryotic cells.

A CRISPR-based dual reporter assay enables genetic mapping of DNA variants that specifically affect mRNA or protein levels in trans.

The bacterium Escherichia coli possesses a permissive cytoplasmic environment and the requisite molecular machinery to support the propagation of prions.

Neuropeptide F/Y from neurons drives rhythmic expression of detoxification-related genes in a peripheral metabolic tissue in flies and mice.

A lack of ADAM10-mediated shedding increases prion protein levels at the plasma membrane and promotes the generation of pathological prion proteins, which accelerates prion disease in mice.

Direct control of ligand binding half-life with light shows that lifetime strongly affects T cell signaling.

Polarized fluorescence microscopy of individual nuclear pores in vivo reveals conformational changes in select domains of proteins of the inner ring.

Cell-type-specific ribosome profiling during prion disease progression identified minor translational changes in neurons as well as profound glia changes many of which are shared with other neurodegenerative diseases.

Sox2 transcription is not correlated with spatial proximity of its essential regulatory enhancer in embryonic stem cells, suggesting gene transcription is not limited to periods of direct enhancer-promoter contact.

A light-controllable ligand is used to probe where in the signaling cascade T cells discriminate self from non-self.