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Fig. 4 | Clinical and Translational Medicine

Fig. 4

From: Mechanoregulation and pathology of YAP/TAZ via Hippo and non-Hippo mechanisms

Fig. 4

Hypothetical models for actomyosin-dependent regulation of YAP nuclear localization in sparse and confluent cells. a Sparse cells develop FAs that are connected to actomyosin stress fibers. Tensile force exertion from stress fibers to FAs activates the FAK–Src signal, which inhibits LATS1/2-mediated phosphorylation of YAP, thereby facilitating nuclear translocation of YAP. In addition, contraction of stress fibers connecting FAs and the apical surface of the nucleus (sometimes called ‘actin cap’) flattens the nucleus, increases the curvature of the lateral part of the nuclear membrane, and thereby enlarges the diameter of the cytoplasmic side of the nuclear pore in this nuclear membrane part. Such ‘asymmetric opening’ of nuclear pores may preferentially promote nuclear import, rather than export, of YAP. b Confluent cells are poor in FAs and stress fibers, but instead develop AJs and actomyosin fibers associated with AJs. Actomyosin-based tensile force at AJs induces translocation of Merlin from AJs to the nucleus, wherein Merlin forms a complex with YAP. With the aid of nuclear export signals of Merlin, the Merlin-YAP complex is then exported from the nucleus. Thus the actomyosin activity has opposing effects on the YAP distribution between sparse and confluent cells; the actomyosin activity promotes nuclear localization of YAP in sparse cells, but attenuates it in confluent cells. See detailed discussion in the main text

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