Hirsch Calley L, Wrana Jeffrey L, Dent Sharon Y R
Center for Systems Biology, Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto M5G 1X5, Canada.
Center for Systems Biology, Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto M5G 1X5, Canada; Department of Molecular Genetics, University of Toronto, Toronto M5S 1A8, Canada.
J Mol Biol. 2017 Jun 30;429(13):1958-1977. doi: 10.1016/j.jmb.2016.09.023. Epub 2016 Oct 6.
Development is generally regarded as a unidirectional process that results in the acquisition of specialized cell fates. During this process, cellular identity is precisely defined by signaling cues that tailor the chromatin landscape for cell-specific gene expression programs. Once established, these pathways and cell states are typically resistant to disruption. However, loss of cell identity occurs during tumor initiation and upon injury response. Moreover, terminally differentiated cells can be experimentally provoked to become pluripotent. Chromatin reorganization is key to the establishment of new gene expression signatures and thus new cell identity. Here, we explore an emerging concept that lysine acetyltransferase (KAT) enzymes drive cellular plasticity in the context of somatic cell reprogramming and tumorigenesis.
发育通常被视为一个单向过程，其结果是获得特定的细胞命运。在此过程中，细胞身份由信号线索精确界定，这些信号线索为细胞特异性基因表达程序调整染色质景观。一旦确立，这些通路和细胞状态通常对破坏具有抗性。然而，在肿瘤发生起始阶段和损伤反应时会发生细胞身份丧失。此外，终末分化细胞可通过实验诱导成为多能细胞。染色质重组是建立新的基因表达特征从而形成新的细胞身份的关键。在这里，我们探讨一个新出现的概念，即赖氨酸乙酰转移酶（KAT）在体细胞重编程和肿瘤发生过程中驱动细胞可塑性。
