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Nature Communications 1 , Article number: 71 doi:10.1038/ncomms1074
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; \4 M9 O4 ^+ {8 Y; g8 _: LNon-muscle myosin II regulates survival threshold of pluripotent stem cells
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. j, |3 X X. z7 u e! uAndrea Walker, Hua Su,Mary Anne Conti,Nicole Harb,Robert S. Adelstein& Noboru Sato$ V4 H7 G) H$ v2 Z, u* ?4 I$ _& ]
1 r% h D$ {) ?& I. A/ jHuman pluripotent stem (hPS) cells such as human embryonic stem (hES) and induced pluripotent stem (hiPS) cells are vulnerable under single cell conditions, which hampers practical applications; yet, the mechanisms underlying this cell death remain elusive. In this paper, we demonstrate that treatment with a specific inhibitor of non-muscle myosin II (NMII), blebbistatin, enhances the survival of hPS cells under clonal density and suspension conditions, and, in combination with a synthetic matrix, supports a fully defined environment for self-renewal. Consistent with this, genetically engineered mouse embryonic stem cells lacking an isoform of NMII heavy chain (NMHCII), or hES cells expressing a short hairpin RNA to knock down NMHCII, show greater viability than controls. Moreover, NMII inhibition increases the expression of self-renewal regulators Oct3/4 and Nanog, suggesting a mechanistic connection between NMII and self-renewal. These results underscore the importance of the molecular motor, NMII, as a novel target for chemically engineering the survival and self-renewal of hPS cells |
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