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Structural, biochemical, and proteomic analyses of a four-subunit core module of the cleavage and polyadenylation specificity factor complex reveal its molecular architecture and specific determinants of polyadenylation signal recognition in human mRNAs.

Idiopathic patients along a complex motor neuron disease-dementia spectrum exhibit mRNA splicing changes that are due to multi-protein insolubility.

Alteration of the G-quadruplex structure formed by GGGGCC repeat RNA through the direct interaction with RNA-binding proteins can suppress pathogenic repeat-associated non-AUG translation, leading to therapeutic effects on neurodegeneration in C9orf72-linked amyotrophic lateral sclerosis and frontotemporal dementia.

Molecular details of the interactions of human Fip1 with CPSF30 and CstF77 unravel key aspects of mRNA polyadenylation and its regulation.

Stem-cell-based neural replacement, in combination with optogenetic stimulation, could represent a translationally viable therapeutic strategy to overcome atrophy and paralysis of targeted muscles in people living with amyotrophic lateral sclerosis.

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

A YTH-domain protein Mmi1 prevents deleterious expression of meiotic proteins by tethering their mRNAs to nuclear foci.

Length-dependent interference of arginine-containing dipeptide repeat proteins with multiple components of the nucleocytoplasmic transport machinery is a potential mechanistic pathway of C9orf72 amyotrophic lateral sclerosis or frontotemporal dementia toxicity.

The localisation of bicoid mRNA depends on its microtubule-independent anchoring at the oocyte anterior.

Self-assembly of bacterial ice nucleation proteins is required for efficient activity and is mediated by electrostatic interactions, creating long and thin fibres.