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.

Excess expression of the Gadd45 mRNA accounts for lethality when nonsense-mediated decay is lost in Drosophila and mammalian cells, revealing that this pathway is a critical gene regulatory mechanism.

RNA polymerase II generates numerous transcript isoforms, including transcripts initiating downstream of the START codon, that are efficiently degraded by the nonsense-mediated mRNA decay pathway.

The nuclear exosome cofactors Mpp6 and Rrp47 can stimulate exoribonuclease activities of the nuclear RNA exosome and recruit the Mtr4 helicase to promote helicase dependent RNA decay.

RNA decay is used at multiple points in the budding yeast unfolded protein response to regulate its suppression and activation, and possibly its attenuation.

A critical component of the cellular response to unfolded proteins is the widespread rescue of ribosomes that stall on endonucleolytically-cleaved mRNA transcripts.

Interconnected RNA processing mechanisms ensure the fidelity of non-conventional mRNA splicing during the unfolded protein response.

A whole-genome siRNA screen identifies ICE1 as a factor required for accurate sensing and quality control of mRNAs containing premature stop codons.

Non-invasive mRNA stability measurements reveal that transcript lifetime is governed by a competition with translation initiation on a transcriptome-wide level.

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