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Significance Taz (transcriptional coactivator with PDZ-binding motif) and Yap (yes-associated protein), the Hippo pathway effector proteins regulating cell fate, organ size, and homeostasis, are targeted by the potent viral oncogene polyomavirus middle T antigen (PyMT). A key process of PyMT is the activation of Src, a cellular proto-oncogene. Remarkably, active Src prevents the Hippo pathway from enhancing Taz decay mediated by its E3-ubiquitin ligase SCF(β-TrCP). We resolved the underlying mechanism by demonstrating that Src inhibits β-TrCP. β-TrCP is a key cellular component regulating a wide range of cellular signaling in cell fate determination. Our discovery of a function of the well-studied Src tyrosine kinase in abrogating β-TrCP function is expected to have wide ramifications for cell fate determination, including in oncogenesis.

The nonreceptor tyrosine kinase c-Src attenuates SCF(β-TrCP) E3-ligase activity abrogating Taz proteasomal degradation