Ribosome collisions along an mRNA are shown to recruit factors that prevent additional ribosomes from initiating translation on that mRNA, thereby providing time to resolve the collision.

Endothelial Differentiation Factor 1 (EDF1) plays a critical role in driving mRNA-specific quality control and global transcriptional responses in response to ribosome collisions.

Collision between ribosomes can cause dissociation of stalled ribosomes from messenger RNAs during the process of mRNA translation.

A model reveals how translation of an mRNA leader could provide resistance to global downregulation of translation.

Without ribosome recycling factor, ribosomes in Escherichia coli accumulate in 3'-UTRs and queue upstream of stop codons, but no effects were observed on the translational coupling of neighboring genes.

The 5' ends of genes are slightly enriched for rare codons largely because the ends turnover in evolution and gather rare codons, and these rare codons do not improve translation.

Genetic screens and functional assays utilizing reporter mRNAs triggering NGD or COMD provide a basis for understanding the unique contributions of each pathway to translation-coupled mRNA decay and contextualizes their effects in the larger cellular process of translation surveillance.

Cue2 is an endonuclease that cleaves mRNA in the A site of the lagging ribosome upon ribosome collision events.

A hierarchical relationship among highly conserved regulatory ribosomal ubiquitylation events and the presence of antagonistic deubiquitylating enzymes suggests a dynamic ubiquitin code impacts ribosome-associated activities.

An eukaryotic specific system cooperates with the ribosome quality control pathway to maintain the reading frame during translation of slowly translated sequences.