Toward pluripotency by reprogramming: mechanisms and application
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Reprogramming
Epigenome
Regenerative Medicine
Cell fate determination
Epigenesis
Maternal stress pre-pregnancy and exposure to stress in utero has life-long negative consequences for the developing foetus. There is growing evidence that this passes through changes in foetal epigenetic markers such as DNA methylation. We hypothesize that the mother's prior life experience and changes in her external environment will change the in utero environment she provides to the developing foetus, and both will be reflected in changes to the mother's epigenome. As classical dogma states that during embryo all DNA methylation marks are removed and replaced de novo, this raises the question as to how to assess the in utero environment, examining the role it plays in the transmission of environmental cues. We suggest that the maternal epigenome can act as a proxy for the developmental environment she provided to her offspring in utero; this developmental environment determines the child's epigenome and lifelong health trajectory. Furthermore, we suggest that the maternal origin of the placental decidua make this the perfect sample for assessing the in utero environment in the context of the mothers' prior life experience, mediating maternal exposure to infant phenotype.
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Over the last decade significant advances have been made toward reprogramming the fate of somatic cells, typically by overexpression of cell lineage-determinant transcription factors. As key regulators of cell fate, the SOX family of transcription factors has emerged as potent drivers of direct somatic cell reprogramming into multiple lineages, in some cases as the sole overexpressed factor. The vast capacity of SOX factors, especially those of the SOXB1, E and F subclasses, to reprogram cell fate is enlightening our understanding of organismal development, cancer and disease, and offers tremendous potential for regenerative medicine and cell-based therapies. Understanding the molecular mechanisms through which SOX factors reprogram cell fate is essential to optimize the development of novel somatic cell transdifferentiation strategies.
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Cell fate conversion by the forced overexpression of transcription factors (TFs) is a process known as reprogramming. It leads to de-differentiation or
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Epigenetic modifications and their regulations govern the identity of every cell type in an organism. Cell differentiation involves a switch in gene expression profile that is accompanied by heritable changes of epigenetic signatures in the differentiated cell type. Differentiation is generally not reversible, thereby conferring cell fate decisions once an altered epigenetic pattern is set. Nevertheless, attempts have been made to reverse a differentiation cell fate to a pluripotent state by various experimental approaches, such as somatic cell nuclear transfer, cell fusion and ectopic expression of defined transcription factors. The fundamental basis of all these strategies is to mediate epigenetic reprogramming, which allows a permanent and completed conversion of cell fate. A comprehensive understanding of the dynamic of epigenetic changes during cell differentiation would provide a more precise and efficient way of reprogramming cell fate. Here we summarize the epigenetic aspects of different reprogramming strategies and discuss the possible mechanisms underlying these epigenetic reprogramming events.
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Cells all share essentially the same genome, which is shaped by the developmental program to bring about various outcomes. It is well known that epigenetic regulation is a key process in determining the different cell functional output from the genetic information. Somatic reprogramming is a dramatic demonstration of this effect, and has opened the gate to the investigation of cell fate determination as cells reverse the developmental program. These studies have revealed which epigenetic marks set during normal development are important for cell specification. Here, we review the epigenetic landmarks that cells pass through during somatic reprogramming, and give an overview to the many remaining unclear epigenetic regulatory events that occurs during reprogramming. © 2016 IUBMB Life, 68(11):854–857, 2016
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Seminal studies by Dr. Shinya Yamanaka revealed that reprogramming technology was able to convert differentiated somatic cells to self-renewing and pluripotent stem cells. Although reprogramming process does not require changes in the genome information, cellular reprogramming elicits dynamic changes of epigenetic regulation. Therefore, reprogramming technology is a powerful tool for the modifying epigenetic regulation. Previous studies have reported that epigenetic regulation plays a critical role on both the development and maintenance of cancer cells. Taking advantage of reprogramming technology, previous studies have actively modified the epigenome of cancer cells and revealed the importance of the coordinated interactions between genetic abnormalities and epigenetic regulation in cancer cells. In this review, we describe advances and challenges in the use of reprogramming technology for studying cancer biology.
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Epigenetic control of gene regulation is fundamental to the maintenance of cellular identities during all stages of metazoan life. Tissue regeneration involves cellular reprogramming processes, like dedifferentiation, re‐differentiation, and trans‐differentiation. Hence, in these processes epigenetic maintenance of gene expression programs requires a resetting through mechanisms that we are only beginning to understand. Here we summarize the current status of these studies, in particular regarding the role of epigenetic mechanisms of cellular reprogramming during tissue regeneration.
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