Division of Molecular and Cellular Biology, Department of Biochemistry and Molecular Biology, Kobe University Graduate School of Medicine, Kobe University, Kobe, Japan.
Division of Cancer Genetics, Department of Molecular Genetics, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
FASEB J. 2019 Apr;33(4):5548-5560. doi: 10.1096/fj.201802005R. Epub 2019 Jan 14.
Cell competition is involved in mammalian embryogenesis and tumor elimination and progression. It was previously shown that, whereas NIH3T3 mouse fibroblasts expressing high levels of the yes-associated protein 1(YAP1) target TEA domain family (TEAD) transcription factors become "winners" in cell competitions, Madin-Darby canine kidney cells expressing activated YAP1 become "losers" and are eliminated from culture monolayers. Thus, YAP1's role in cell competitions is clearly context dependent. Here, we show that keratinocytes overexpressing a constitutively activated YAP1 mutant lose in in vitro competitions with control cells conducted in standard tissue culture dishes and undergo apical extrusion. Similarly, cells in which endogenous YAP1 is activated by NF2 knockdown become losers. The YAP1-overexpressing cells exhibit a decrease in cell-matrix adhesion because of defective expression of adhesion molecules such as fibronectin-1. Cell adhesion-mediated proliferation is also impaired. However, because of intrinsic factors, YAP1-expressing cells proliferate faster than control cells when cocultured in dishes impeding cell adhesion. In vivo, Mob1a/b-deficient (YAP1-activated) epidermis, which shows decreased expression of type XVII collagen, cannot be engrafted successfully onto donor mice. YAP1-activated skin grafts shrink away from surrounding control skin, and the epidermis peels off the basement membrane. Our data show that YAP1 activation controls cell competition in part by decreasing cell adhesion.-Nishio, M., Miyachi, Y., Otani, J., Tane, S., Omori, H., Ueda, F., Togashi, H., Sasaki, T., Mak, T. W., Nakao, K., Fujita, Y., Nishina, H., Maehama, T., Suzuki, A. Hippo pathway controls cell adhesion and context-dependent cell competition to influence skin engraftment efficiency.
细胞竞争参与哺乳动物胚胎发生和肿瘤消除及进展。先前的研究表明,在表达高水平 yes 相关蛋白 1(YAP1)的 NIH3T3 小鼠成纤维细胞中,YAP1 靶向 TEA 结构域家族(TEAD)转录因子,这些细胞成为细胞竞争的“胜者”,而表达激活型 YAP1 的犬肾 Madin-Darby 细胞则成为“败者”,并从培养单层中被清除。因此,YAP1 在细胞竞争中的作用显然是依赖于上下文的。在这里,我们发现,过表达组成性激活 YAP1 突变体的角质形成细胞在标准组织培养皿中进行的与对照细胞的体外竞争中失败,并发生顶端挤出。同样,内源性 YAP1 被 NF2 敲低激活的细胞也成为败者。由于粘附分子(如纤连蛋白 1)的表达缺陷,YAP1 过表达细胞的细胞-基质粘附减少。细胞粘附介导的增殖也受损。然而,由于内在因素,当与抑制细胞粘附的培养皿共培养时,YAP1 表达细胞比对照细胞增殖更快。在体内,Mob1a/b 缺陷(YAP1 激活)表皮显示 XVII 型胶原表达减少,不能成功移植到供体小鼠上。YAP1 激活的皮肤移植物从周围对照皮肤退缩,表皮从基底膜剥离。我们的数据表明,YAP1 激活通过降低细胞粘附来部分控制细胞竞争。