Open Close
Reference
Citation
Udan, R.S., Kango-Singh, M., Nolo, R., Tao, C., Halder, G. (2003). Hippo promotes proliferation arrest and apoptosis in the Salvador/Warts pathway.  Nat. Cell Biol. 5(10): 914--920.
FlyBase ID
FBrf0167938
Publication Type
Research paper
Abstract
Proliferation and apoptosis must be precisely regulated to form organs with appropriate cell numbers and to avoid tumour growth. Here we show that Hippo (Hpo), the Drosophila homologue of the mammalian Ste20-like kinases, MST1/2, promotes proper termination of cell proliferation and stimulates apoptosis during development. hpo mutant tissues are larger than normal because mutant cells continue to proliferate beyond normal tissue size and are resistant to apoptotic stimuli that usually eliminate extra cells. Hpo negatively regulates expression of Cyclin E to restrict cell proliferation, downregulates the Drosophila inhibitor of apoptosis protein DIAP1, and induces the proapoptotic gene head involution defective (hid) to promote apoptosis. The mutant phenotypes of hpo are similar to those of warts (wts), which encodes a serine/threonine kinase of the myotonic dystrophy protein kinase family, and salvador (sav), which encodes a WW domain protein that binds to Wts. We find that Sav binds to a regulatory domain of Hpo that is essential for its function, indicating that Hpo acts together with Sav and Wts in a signalling module that coordinately regulates cell proliferation and apoptosis.
PubMed ID
PubMed Central ID
Related Publication(s)
Note
Hippo and its mission for growth control.
Ryoo and Steller, 2003, Nat. Cell Biol. 5(10): 853--855 [FBrf0167935]
Associated Information
Comments
Associated Files
Other Information
Secondary IDs
    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Nat. Cell Biol.
    Title
    Nature Cell Biology
    Publication Year
    1999-
    ISBN/ISSN
    1465-7392 1476-4679
    Data From Reference
    Alleles (17)
    Gene Groups (1)
    Genes (15)
    Physical Interactions (3)
    Natural transposons (1)
    Insertions (1)
    Experimental Tools (1)
    Transgenic Constructs (6)