西亚试剂：Integrated biochemical and mechanical signals regulate mult

Integrated biochemical and mechanical signals regulate multifaceted human embryonic stem cell functions
Dong Li1,2, Jiaxi Zhou1,2, Lu Wang1,2, Myung Eun Shin1,2, Pei Su1,2, Xiaohua Lei5, Haibin Kuang5, Weixiang Guo5, Hong Yang1,2, Linzhao Cheng6, Tetsuya S. Tanaka1,3, Deborah E. Leckband4, Albert B. Reynolds7, Enkui Duan5, and Fei Wang1,2

1Institute for Genomic Biology, 2Department of Cell and Developmental Biology, 3Department of Animal Sciences, and 4Department of Chemical and Molecular Engineering, University of Illinois at Urbana-Champaign, Urbana, IL 61801
5State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Science, Beijing 100101, China
6Stem Cell Program, Institute for Cell Engineering, School of Medicine, Johns Hopkins University, Baltimore, MD 21205
7Department of Cancer Biology, Vanderbilt University, Nashville, TN 37232

Human embryonic stem cells (ESCs [hESCs]) proliferate as colonies wherein individual cells are strongly adhered to one another. This architecture is linked to hESC self-renewal, pluripotency, and survival and depends on epithelial cadherin (E-cadherin), NMMIIA (nonmuscle myosin IIA), and p120-catenin. E-cadherin and p120-catenin work within a positive feedback loop that promotes localized accumulation of E-cadherin at intercellular junctions. NMMIIA stabilizes p120-catenin protein and controls E-cadherin–mediated intercellular adhesion. Perturbations of this signaling network disrupt colony formation, destabilize the transcriptional regulatory circuitry for pluripotency, and impair long-term survival of hESCs. Furthermore, depletion of E-cadherin markedly reduces the efficiency of reprogramming of human somatic cells to an ESC-like state. The feedback regulation and mechanical–biochemical integration provide mechanistic insights for the regulation of intercellular adhesion and cellular architecture in hESCs during long-term self-renewal. Our findings also contribute to the understanding of microenvironmental regulation of hESC identity and somatic reprogramming.

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