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Symmetry from Asymmetry or Asymmetry from Symmetry?

机译:从非对称对称还是从对称非对称?

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摘要

The processes of DNA replication and mitosis allow the genetic information of a cell to be copied and transferred reliably to its daughter cells. However, if DNA replication and cell division were always carried out in a symmetric manner, it would result in a cluster of tumor cells instead of a multicellular organism. Therefore, gaining a complete understanding of any complex living organism depends on learning how cells become different while faithfully maintaining the same genetic material. It is well recognized that the distinct epigenetic information contained in each cell type defines its unique gene expression program. Nevertheless, how epigenetic information contained in the parental cell is either maintained or changed in the daughter cells remains largely unknown. During the asymmetric cell division (ACD) of Drosophila male germline stem cells (GSCs), our previous work revealed that preexisting histones are selectively retained in the renewed stem cell daughter, whereas newly synthesized histones are enriched in the differentiating daughter cell. We also found that randomized inheritance of preexisting histones versus newly synthesized histones results in both stem cell loss and progenitor germ cell tumor phenotypes, suggesting that programmed histone inheritance is a key epigenetic player for cells to either remember or reset cell fates. Here we will discuss these findings in the context of current knowledge on DNA replication, polarized mitotic machinery, and ACD for both animal development and tissue homeostasis. We will also speculate on some potential mechanisms underlying asymmetric histone inheritance, which may be used in other biological events to achieve the asymmetric cell fates.
机译:DNA复制和有丝分裂的过程使细胞的遗传信息得以复制并可靠地转移到其子细胞。但是,如果DNA复制和细胞分裂始终以对称方式进行,则会导致肿瘤细胞簇而不是多细胞生物。因此,全面了解任何复杂的活生物体都取决于学习细胞如何变得不同,同时忠实地维持相同的遗传物质。众所周知,每种细胞类型中包含的独特的表观遗传信息定义了其独特的基因表达程序。然而,在子细胞中如何维持或改变亲代细胞中所含的表观遗传信息仍然是未知的。在果蝇雄性生殖系干细胞(GSC)的不对称细胞分裂(ACD)期间,我们以前的工作表明,先前存在的组蛋白选择性地保留在更新的干细胞子代中,而新合成的组蛋白则富集在分化的子代细胞中。我们还发现,先前存在的组蛋白与新合成的组蛋白的随机遗传会导致干细胞丢失和祖先生殖细胞肿瘤表型,这表明程序化组蛋白遗传是细胞记忆或重置细胞命运的关键表观遗传参与者。在这里,我们将在动物复制和组织稳态方面有关DNA复制,极化有丝分裂机制和ACD的当前知识的背景下讨论这些发现。我们还将推测不对称组蛋白遗传的一些潜在机制,这些机制可能用于其他生物学事件中以实现不对称细胞命运。

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