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How do mammalian cells that share the same genome exist in notably distinctphenotypes, exhibiting differences in morphology, gene expression patterns, andepigenetic chromatin statuses? Furthermore how do cells of different phenotypesdifferentiate reproducibly from a single fertilized egg? These fundamentalquestions are closely related to a deeply rooted paradigm in developmentalbiology that cell differentiation is irreversible. Yet, recently a growing bodyof research suggests the possibility of cell reprogramming, which offers thepotential for us to convert one type of cell into another. Despite thesignificance of quantitative understandings of cell reprogramming, theoreticalefforts often suffer from the complexity of large circuits maintaining cellphenotypes coupled at many different epigenetic and gene regulation levels. Tocapture the global architecture of cell phenotypes, we propose an "epigeneticstate network" approach that translates the classical concept of an epigeneticlandscape into a simple-yet-predictive mathematical model. As a testing case,we apply the approach to the reprogramming of fibroblasts (FB) tocardiomyocytes (CM). The epigenetic state network for this case predicts threemajor pathways of reprogramming. One pathway goes by way of induced pluripotentstem cells (iPSC) and continues on to the normal pathway of cardiomyocytedifferentiation. The other two pathways involve transdifferentiation (TD)either indirectly through cardiac progenitor (CP) cells or directly fromfibroblast to cardiomyocyte. Numerous experimental observations support thepredicted states and pathways.

Global Epigenetic State Network Governs Cellular Pluripotent Reprogramming and Transdifferentiation