Institut de Biologia Molecular de Barcelona, Consejo Superior de Investigaciones Científicas, Parc Científic de Barcelona, Baldiri i Reixac 4, E-08028 Barcelona, Spain.
Center for Regenerative Medicine in Barcelona, Doctor Aiguader 88, E-08003, Barcelona, Spain.
J Biol Chem. 2011 Oct 14;286(41):35347-35357. doi: 10.1074/jbc.M111.281923. Epub 2011 Aug 18.
There are seven linker histone variants in human somatic cells (H1.0 to H1.5 and H1X), and their prevalence varies as a function of cell type and differentiation stage, suggesting that the different variants may have distinct roles. We have revisited this notion by using new methodologies to study pluripotency and differentiation, including the in vitro differentiation of human embryonic stem (ES) and teratocarcinoma cells and the reprogramming of keratinocytes to induced pluripotent stem cells. Our results show that pluripotent cells (PCs) have decreased levels of H1.0 and increased levels of H1.1, H1.3, and H1.5 compared with differentiated cells. PCs have a more diverse repertoire of H1 variants, whereas in differentiated cells, H1.0 expression represents ∼80% of the H1 transcripts. In agreement with their prevalent expression in ES cells, the regulatory regions of H1.3 and H1.5 genes were found to be occupied by pluripotency factors. Moreover, the H1.0 gene promoter contains bivalent domains (H3K4me2 and H3K27me3) in PCs, suggesting that this variant is likely to have an important role during differentiation. Indeed, the knockdown of H1.0 in human ES did not affect self-renewal but impaired differentiation. Accordingly, H1.0 was recruited to the regulatory regions of differentiation and pluripotency genes during differentiation, confirming that this histone variant plays a critical role in the regulation of these genes. Thus, histone H1 variant expression is controlled by a variety of mechanisms that produce distinct but consistent H1 repertoires in pluripotent and differentiated cells that appear critical to maintain the functionality of such cells.
在人类体细胞中有七种连接组蛋白变体(H1.0 到 H1.5 和 H1X),它们的流行程度随细胞类型和分化阶段而异,这表明不同的变体可能具有不同的作用。我们使用新的方法学重新研究了这个概念,包括体外分化人类胚胎干细胞(ES)和畸胎瘤细胞以及将角质形成细胞重编程为诱导多能干细胞,以研究多能性和分化。我们的结果表明,与分化细胞相比,多能细胞(PCs)的 H1.0 水平降低,而 H1.1、H1.3 和 H1.5 水平升高。PCs 具有更多种类的 H1 变体,而在分化细胞中,H1.0 表达占 H1 转录本的约 80%。与 H1.3 和 H1.5 基因在 ES 细胞中的普遍表达一致,它们的调控区域被多能性因子占据。此外,在 PC 中,H1.0 基因启动子含有多价结构域(H3K4me2 和 H3K27me3),这表明该变体在分化过程中可能具有重要作用。事实上,在人类 ES 中敲低 H1.0 并不影响自我更新,但会损害分化。因此,H1.0 在分化过程中被招募到分化和多能性基因的调控区域,证实该组蛋白变体在这些基因的调控中起着关键作用。因此,组蛋白 H1 变体的表达受到多种机制的控制,这些机制在多能性和分化细胞中产生不同但一致的 H1 谱,这对于维持这些细胞的功能似乎至关重要。