Regulation of conserved Nodal factors by a maternal protein ensures that Nodal signaling is repressed until the appropriate time in embryonic development.
Non-invasive mRNA stability measurements reveal that transcript lifetime is governed by a competition with translation initiation on a transcriptome-wide level.
A poly(A) tail-based regulatory mechanism dynamically controls PABPC1 protein synthesis in cardiomyocytes and thereby titrates cellular translation in response to developmental and hypertrophic cues.
In mouse cardiomyocytes, (lymph)angiogenic growth factors are induced during early hypoxia by a translational mechanism involving a new IRES trans-acting factor, vasohibin-1.
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.
The unspliced HAC1 mRNA does not give rise to detectable protein in budding yeast, despite its cytoplasmic localization, due to a two-part post-transcriptional silencing mechanism.