The Hippo pathway downstream effector YAP regulates S-phase progression to protect neural stem cells of the retina from experiencing genomic instability.
High levels of nuclear YAP are sufficient to drive squamous cell carincoma formation and frequently also drive progression to spindle cell carcinoma by promoting epithelial-to-mesenchymal transition after tissue damage.
As the first fully genetically encoded method, PARIS allows cell-specific, long-term, repeated measurements of gap junctional coupling with high spatiotemporal resolution, facilitating its study in both health and disease.
Gap junctions exist in Kenyon cells and Kenyon cell-mushroom body output neuron neural networks, and are also critical in visual learning and memory in Drosophila.
Coordination between crossover designation and synaptonemal complex disassembly is executed via a conserved MAP kinase pathway and is critical for accurate chromosome segregation during meiosis.
Genetic study of C. elegans neural development reveals the function of glia-neuron gap junctions in neuronal axon specification, and shows that glial cells regulate neuronal intracellular pathways through gap junctions.
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.
