Ribosome profiling reveals genome-wide stimulation of stop codon readthrough by aminoglycosides that is influenced sequence context.

A close approximation to the successor representation is learnt by a simple spike-time-dependent learning rule between cells undergoing theta phase precession.

Ribosomes translate through stop codons far more often than previously thought, yielding C-terminally extended proteins in a variety of eukaryotes.

Natural step-to-step variations show how human running is stabilized, underscoring the importance of center of mass control and showing how humans run without falling despite muscle noise and uneven terrain.

Glial TDP-43 regulates splicing and expression of neurofascin and is required for proper assembly and maintenance of paranodal axoglial junctions.

A nuclear Non-stop identity complex (NIC) supervises enterocyte (EC) identity, preserves tissue homeostasis, and prevents premature aging by maintaining EC-specific gene expression, silencing non-relevant programs, and safeguarding large-scale nuclear organization.

Loss of the RNA-binding protein TDP-43 impairs the survival of oligodendrocyte progenitors and reactivates growth of mature oligodendrocytes, resulting in inappropriate wrapping of neuronal somata and blood vessels.

Impairing TDP-43 RNA-binding capacity through a single acetylation-mimic mutation alters TDP-43 function and recapitulates biochemical, molecular, and behavioral features of sporadic TDP-43 proteinopathies, thus providing opportunities for new research into pathogenic mechanisms and therapeutic interventions.

An unbiased biochemical screen reveals a direct link between gene regulation and actin cytoskeleton remodeling.

The RNA-mediated higher order assembly of TDP-43, a protein associated with neurodegenerative diseases, preserves its solubility by reducing the risk of multivalent interactions between low complexity domains.