Hippo pathway signaling and YAP/TAZ

The paper identifies Tead-Yap regulation of pluripotency factors and cell competition in epiblast formation, showing Tead activity drives pluripotency and eliminates unspecified cells.

The paper investigates how the acto-myosin system regulates YAP activity during liver regeneration in response to bile acid overload.

This study shows that the LATS/YAP/TAZ pathway regulates SOX2+ pituitary stem cells, controlling their homeostasis and tumourigenic potential during development and in adulthood.

This study shows that deleting Lats1 and Lats2 in adult mouse pancreatic acinar cells causes fibrosis and inflammation through YAP1/TAZ activation.

This study shows that YAP/TAZ deletion in mouse neural progenitor cells causes hydrocephalus, disrupts cell polarity, increases cell cycle exit, and reduces differentiation into Tbr2+ cells.

The paper shows HIPPO signaling resolves cell fate conflicts by repositioning cells during pluripotency establishment in the mouse embryo.

This study identifies Shavenbaby as a novel Hippo pathway effector critical for adult stem cell survival by activating DIAP1 to prevent apoptosis in Drosophila renal stem cells.

This study shows Yap regulates glucose utilization and nucleotide synthesis to support organ growth in zebrafish, with conserved mechanisms in mammals.

The paper shows the Drosophila testis niche controls stem cell proliferation by repressing Hippo pathway genes without involving a binary fate decision between stemness and differentiation.

This study shows Amot and Yap1 regulate dendritic tree morphogenesis in neurons, with Amot mediating this process through interactions with Yap1.

This study identifies mechanisms regulating YAP1 nuclear shuttling in fibroblasts, showing that Src and actomyosin suppress YAP1 export, and nuclear export is central to YAP1 regulation.

This study shows that YAP activity drives WNT16/{beta}-catenin signaling to promote keratinocyte proliferation in murine skin, identifying WNT16 as a paracrine ligand in this process.

This study shows YAP and TAZ regulate endothelial cell dynamics and vascular development by modulating junctions and signaling pathways.

This study identifies Taz as essential for micropylar cell specification and micropyle formation in zebrafish through genetic and molecular analysis.

This study shows YAP and TAZ redundantly promote bone development by regulating collagen I expression and organization through TEAD4 binding.