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Most oncogenes, however, require a combination of at least two signals to promote proliferation. In this study, we present evidence that Yap activation is insufficient to promote growth in the otherwise normal tissue. Using a mosaic mouse model, we demonstrate that Yap overexpression in a fraction of hepatocytes does not lead to their clonal expansion, as proliferation is counterbalanced by increased apoptosis. To shift the activity of Yap towards growth, a second signal provided by tissue damage or inflammation is required. In response to liver injury, Yap drives clonal expansion, suppresses hepatocyte differentiation, and promotes a progenitor phenotype. These results suggest that Yap activation is insufficient to promote growth in the absence of a second signal thus coordinating tissue homeostasis and repair.<\/jats:p>","DOI":"10.7554\/elife.02948","type":"journal-article","created":{"date-parts":[[2015,2,10]],"date-time":"2015-02-10T07:32:44Z","timestamp":1423553564000},"source":"Crossref","is-referenced-by-count":61,"title":["Two-signal requirement for growth-promoting function of Yap in hepatocytes"],"prefix":"10.7554","volume":"4","author":[{"given":"Tian","family":"Su","sequence":"first","affiliation":[{"name":"Department of Immunobiology, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, United States"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tanya","family":"Bondar","sequence":"additional","affiliation":[{"name":"Department of Immunobiology, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, United 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