Mitochondria can tune the protein synthesis of nuclear-encoded proteins through condition-dependent mRNA localization that is regulated by translation elongation and the geometric constraints of the cell.
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.
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.
Skd3 (human ClpB) is a potent ATP-dependent mitochondrial protein disaggregase that is activated by the rhomboid protease, PARL, and inactivated by MGCA7-linked mutations.
The reduced ability of Drosophila imaginal discs to regenerate as they mature can be explained by the silencing of damage-responsive enhancers that regulate expression of genes required for regeneration.
Adaptations in protein synthesis and mRNA surveillance machinery enabled the malaria-causing parasite P. falciparum to efficiently and accurately translate long polyA nucleotide runs into long poly-lysine peptides.
Extensive molecular profiling shows how loss of highly similar, paralogous ribosomal proteins lead to distinct phenotypic outputs, through translational control of specific mRNAs.
Genetic analyses reveal that the loss of Lin28a causes axial shortening with mild skeletal transformations via decreased PRC1 at Hox genes, establishing a new pathway in the “Hox code.”.
