Genetic and bioinformatic analyses uncover an unexpected role for codon usage biases in regulating gene expression at the transcriptional level by suppressing premature transcription termination.

microRNAs can serve as a surveillance system to repress nonsense mRNAs by recognizing miRNA-responsive elements in the open reading frame region downstream of the premature termination codon.

Nucleotide resolution mapping of ribosome-bound RNA decay fragments in yeast cells expressing ATPase-deficient UPF1 reveals 3' UTR bound ribosomes and a role for UPF1 in post-termination ribosome recycling.

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

Ribosomes undergo an unanticipated movement (‘sliding’) while translating homopolymeric A sequences, which provides a biochemical rationale for the observation that iterated AAA codons are under-represented in gene-coding sequences.

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

Nonstop mRNA decay degrades mRNAs with a premature stop codon after such mRNAs are targeted by the nonsense-mediated decay machinery.

The RNA-binding protein PTBP1 is recruited to sites near stop codons in retroviral and human mRNAs, shielding them from detection and degradation by the nonsense-mediated mRNA decay pathway.

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

Cells resolve unassigned codons with near-cognate suppression, frameshifting, and ribosomal rescue mechanisms, demonstrating that unassigned codons are permissible in both natural and engineered genetic codes as barriers to horizontal gene transfer.