Blog
About

29
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      The Hippo signaling pathway coordinately regulates cell proliferation and apoptosis by inactivating Yorkie, the Drosophila Homolog of YAP.

      Cell

      metabolism, Transcription Factors, physiology, Cell Proliferation, Drosophila, Drosophila Proteins, antagonists & inhibitors, genetics, Apoptosis, Intracellular Signaling Peptides and Proteins, MAP Kinase Kinase Kinases, Molecular Sequence Data, Nuclear Proteins, Phenotype, Phosphoproteins, Phosphorylation, Photoreceptor Cells, Invertebrate, abnormalities, growth & development, Protein Kinases, Protein-Serine-Threonine Kinases, Saccharomyces cerevisiae Proteins, Signal Transduction, Trans-Activators, Amino Acid Sequence, Animals

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Coordination between cell proliferation and cell death is essential to maintain homeostasis in multicellular organisms. In Drosophila, these two processes are regulated by a pathway involving the Ste20-like kinase Hippo (Hpo) and the NDR family kinase Warts (Wts; also called Lats). Hpo phosphorylates and activates Wts, which in turn, through unknown mechanisms, negatively regulates the transcription of cell-cycle and cell-death regulators such as cycE and diap1. Here we identify Yorkie (Yki), the Drosophila ortholog of the mammalian transcriptional coactivator yes-associated protein (YAP), as a missing link between Wts and transcriptional regulation. Yki is required for normal tissue growth and diap1 transcription and is phosphorylated and inactivated by Wts. Overexpression of yki phenocopies loss-of-function mutations of hpo or wts, including elevated transcription of cycE and diap1, increased proliferation, defective apoptosis, and tissue overgrowth. Thus, Yki is a critical target of the Wts/Lats protein kinase and a potential oncogene.

          Related collections

          Author and article information

          Journal
          10.1016/j.cell.2005.06.007
          16096061

          Comments

          Comment on this article