YAP (yes-associated protein) and TAZ are oncogenic transcriptional co-activators downstream of the Hippo tumor-suppressor pathway. However, whether YAP and/or TAZ (YAP/TAZ) engage in transcriptional co-repression remains relatively unexplored. Here, we directly demonstrated that YAP/TAZ represses numerous target genes, including tumor-suppressor genes such as DDIT4 (DNA-damage-inducible transcript 4) and Trail (TNF-related apoptosis-inducing ligand). Mechanistically, the repressor function of YAP/TAZ requires TEAD (TEA domain) transcription factors. A YAP/TAZ-TEAD complex recruits the NuRD complex to deacetylate histones and alters nucleosome occupancy at target genes. Functionally, repression of DDIT4 and Trail by YAP/TAZ is required for mTORC1 (mechanistic target of rapamycin complex 1) activation and cell survival, respectively. Our demonstration of the transcriptional co-repressor activity of YAP/TAZ opens a new avenue for understanding the Hippo signaling pathway.

Hydrolysis of In(O-iPr)3 by 10 molar excess of water at 90 degrees C in a surfactant/solvent mixture of oleylamine/oleic acid/trioctylamine provides very small nanoparticles (<5 nm in diameter) of In(O)(OH). Subsequent in situ thermolysis of the formed In(O)(OH) nanoparticles at 350 degrees C and ambient pressure produces monodisperse h-In2O3 nanocubes, which can form an extended two-dimensional array on a flat surface. The size of the In2O3 nanocubes (8, 10, and 12 nm) could be easily controlled by the simple change in the amounts of employed surfactants. The h-In2O3 nanocube samples show blue PL emissions at room temperature due to, presumably, systematic oxygen vacancy.