The dynamics of chromatin states mediated by epigenetic modifications during somatic cell reprogramming

Abstract

Somatic cell reprogramming (SCR) is the conversion of differentiated somatic cells into totipotent or pluripotent cells through a variety of methods. Somatic cell reprogramming also provides a platform to investigate the role of chromatin-based factors in establishing and maintaining totipotency or pluripotency, since high expression of totipotency- or pluripotency-related genes usually require an active chromatin state. Several studies in plants or mammals have recently shed light on the molecular mechanisms by which epigenetic modifications regulate the expression of totipotency or pluripotency genes by altering their chromatin states. In this review, we present a comprehensive overview of the dynamic changes in epigenetic modifications and chromatin states during reprogramming from somatic cells to totipotent or pluripotent cells. In addition, we illustrate the potential role of DNA methylation, histone modifications, histone variants, and chromatin remodeling during somatic cell reprogramming, which will pave the way to developing reliable strategies for efficient cellular reprogramming.

Participation of the TBP‐associated factors (TAFs) in cell differentiation

“…A major issue in Developmental Biology is to understand the mechanisms that regulate gene expression for determining cell lineages and the onset of terminal differentiation. These processes consist in a spatiotemporal control that depends upon a collection of processes that involve the participation of (i) transcription factors and their interaction with housekeeping and specific promoters and enhancers (Russo et al, 2018), (ii) chromatin remodeling complexes (Chen et al, 2023), (iii) the epigenetic machinery for DNA and histone modifications (Joseph & Young, 2023; Peng et al, 2023), and (iv) posttranscriptional regulation by noncoding RNAs (Hunkler et al, 2022; Van Wijk et al, 2022). Together, they allow the expression of different phenotypes during embryogenesis, the development of specialized cell types, and the establishment of stem cell reservoirs in mature individuals.…”

Involvement of the H3.3 Histone Variant in the Epigenetic Regulation of Gene Expression in the Nervous System, in Both Physiological and Pathological Conditions

“…The chromatin structure is highly dynamic and changes in different cells during development and differentiation; it also changes in terminally differentiated cells in response to specific inducing factors, such as, for example, thyroid or steroid hormones [11]. At least three connected mechanisms are known to induce structural rearrangements of chromatin (Figure 1): (i) post-translational modification (PTM) of histone proteins [10,12] together with DNA methylation [10,13,14]; (ii) the activity of ATP-dependent complexes that are able to induce modifications in the structure/position of nucleosomes [15], and, finally, (iii) the synthesis and incorporation of histone variants into chromatin [7,[16][17][18]. Herein, we will mainly focus on the latter mechanism (Figure 1, pathway c) and, in particular, on the specific involvement of the H3 histone variant, known as H3.3 core histone, in the epigenetic regulation of gene expression in the nervous system during maturation, as well as in the acquisition of complex functions such as learning and memory.…”

“…The chromatin structure is highly dynamic and changes in different cells during development and differentiation; it also changes in terminally differentiated cells in response to specific inducing factors, such as, for example, thyroid or steroid hormones [ 11 ]. At least three connected mechanisms are known to induce structural rearrangements of chromatin ( Figure 1 ): (i) post-translational modification (PTM) of histone proteins [ 10 , 12 ] together with DNA methylation [ 10 , 13 , 14 ]; (ii) the activity of ATP-dependent complexes that are able to induce modifications in the structure/position of nucleosomes [ 15 ], and, finally, (iii) the synthesis and incorporation of histone variants into chromatin [ 7 , 16 , 17 , 18 ].…”