Activation of the integrated stress response by stalled translation elongation complexes attenuates neurodegeneration, and demonstrates a protective link between a decrease in the rate of translation initiation and defects in translation elongation.
The kinase that controls maternal mRNA translation is regulated by phosphorylation of its activating subunit to restrict kinase activity to the developmental window between meiosis completion and early embryogenesis.
SMAD1/5 signaling is essential for the full transforming growth factor β (TGF-β)-induced transcriptional program and physiological responses and is induced via a novel receptor activation mechanism, involving two distinct type I receptors.
Activation of the stress response pathway in young cells extends replicative lifespan, not by reducing global protein synthesis per se, but by Gcn4-mediated autophagy induction.
Pre-existing enhancers interpret T cell signaling strength in an analogue manner to direct quantitative changes in gene expression within the context of an overall digital response.
Overexpression of PLK1 triggers oncogenic transformation and transcriptional reprogramming of prostate epithelial cells, which stimulates cell migration and invasion.
In fruit flies, maternally deposited RNA-binding proteins are removed during the maternal-to-zygotic transition via a mechanism of translational upregulation of Kondo, the key E2 enzyme, at egg activation.
Drosophila melanogaster embryos undergo a dramatic genomic transformation in the hour preceding gastrulation, as thousands of promoters and regulatory regions become biochemically distinct before they become active.
During ES cell differentiation, Yap1 directly regulates apoptosis-related genes like Bcl-2 and Mcl-1 to attenuate apoptosis and promote cell survival to allow for successful cell fate changes.
A model of signalling pathways interacting with proneural gene expression explains the sequential patterning of the largest visual processing centre in the developing Drosophila brain.
