Cell competition is an important mechanism selecting against aneuploid cells.

Minimal changes allow an ancestral, unfolded peptide to adopt a known fold by repetition, illuminating a possible path for the emergence of folded proteins at the origin of life.

Signalling that maintains rapid translation elongation in KRAS-mutant colorectal cancer models can be targeted by mutation of the ribosomal protein RPL24 to suppress tumour proliferation.

Two integrated approaches shed light on how XBP1 arrest peptide induces intermediate level of translational pausing and identify hotspot positions to make it stronger.

Cooperativity between two transcription regulators occurs through protein-protein interactions with a general transcription factor complex and potentiates the parallel evolution of their DNA binding sites.

The homozygous and heterozygous phenotypes of mouse Rps12 deletion are described, highlighting pancytopenia reflecting roles in hematopoiesis and erythropoiesis.

A structural element of mRNA exit channel protein Rps5 performs a critical role in start codon recognition during translation initiation by stabilizing initiator tRNA binding to the pre-initiation complex.

A newly discovered mechanism that causes the 'Minute' phenotype in fruit flies can explain how organisms are able to eliminate the mutant cells that arise occasionally during development.

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

Ribosomal protein mutations, mutations that affect ribosomal RNA synthesis, or function of the mature ribosome, trigger a transcriptional response mediated by Xrp1 expression which reduces cellular translation via eIF2-alpha phosphorylation and renders cells liable to competition with wild-type neighbors.