Myogenic transcriptional activation of
            <i>MyoD</i>
            mediated by replication-independent histone deposition

Yang, Jae Hyuk; Song, Young-Gi; Seol, Ja Hwan; Park, Jin Young; Yang, Yong; Han, Jeung Whan; Youn, Hong Duk; Cho, Eun Jung

doi:10.1073/pnas.1009830108

Cited by 82 publications

(97 citation statements)

References 50 publications

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“…For example, H3.3 is important for early gene activation in cell lines and during myogenic differentiation (Placek et al 2009;Tamura et al 2009;Yang et al 2011). In Xenopus, HIRA-mediated deposition of H3.3 is required for the transcriptional memory of active genes after somatic cell transfer into enucleated eggs (Ng and Gurdon 2008;Jullien et al 2012).…”

Section: H33: a Dynamic Memorymentioning

confidence: 99%

Histone variants: dynamic punctuation in transcription

2014

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Eukaryotic gene regulation involves a balance between packaging of the genome into nucleosomes and enabling access to regulatory proteins and RNA polymerase. Nucleosomes are integral components of gene regulation that restrict access to both regulatory sequences and the underlying template. Whereas canonical histones package the newly replicated genome, they can be replaced with histone variants that alter nucleosome structure, stability, dynamics, and, ultimately, DNA accessibility. Here we consider how histone variants and their interacting partners are involved in transcriptional regulation through the creation of unique chromatin states.

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Section: H33: a Dynamic Memorymentioning

confidence: 99%

Histone variants: dynamic punctuation in transcription

2014

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“…HIRA also plays a critical role in early developmental processes: null embryos exhibit lethality by E10-11 due to defects that begin during gastrulation at E6 and alter subsequent formation of the mesoderm and primitive streak (19). This can alter expression of important tissue-restricted regulators in development, such as MyoD during myogenic differentiation (56) and VEGFR1 in vascular development and angiogenesis (52). Analogous to our observations showing that erythroid lineage differentiation (EKLF, GATA-1, and β-globin) but not early hematopoiesis (GATA-2) is affected, HIRA-null ES cells are able to generate neuronal precursor cells but not mature neurons (47).…”

Section: Discussionmentioning

confidence: 99%

Transcription factor EKLF (KLF1) recruitment of the histone chaperone HIRA is essential for β-globin gene expression

Soni

Pchelintsev

Adams

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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The binding of chromatin-associated proteins and incorporation of histone variants correlates with alterations in gene expression. These changes have been particularly well analyzed at the mammalian β-globin locus, where transcription factors such as erythroid Krüppel-like factor (EKLF), which is also known as Krüppel-like factor 1 (KLF1), play a coordinating role in establishing the proper chromatin structure and inducing high-level expression of adult β-globin. We had previously shown that EKLF preferentially interacts with histone H3 and that the H3.3 variant is differentially recruited to the β-globin promoter. We now find that a novel interaction between EKLF and the histone cell cycle regulation defective homolog A (HIRA) histone chaperone accounts for these effects. HIRA is not only critical for β-globin expression but is also required for activation of the erythropoietic regulators EKLF and GATA binding protein 1 (GATA1). Our results provide a mechanism by which transcription factor-directed recruitment of a generally expressed histone chaperone can lead to tissue-restricted changes in chromatin components, structure, and transcription at specific genomic sites during differentiation.

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“…It is important for the differentiation of C2C12 myoblasts into myotubes (Song et al, 2012). HIRA facilitates expression of Myod1 through incorporation of histone H3.3 into its promoter and enhancer regions (Yang et al, 2011b). Histone H3.3 itself epigenetically maintains expression of the Myod1 gene after cell division (Ng and Gurdon, 2008).…”

Section: Discussionmentioning

confidence: 99%

HIRA deficiency in muscle fibers causes hypertrophy and susceptibility to oxidative stress

Valenzuela

Soibam

et al. 2017

Journal of Cell Science

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Nucleosome assembly proceeds through DNA replication-coupled or replication-independent mechanisms. For skeletal myocytes, whose nuclei have permanently exited the cell cycle, replicationindependent assembly is the only mode available for chromatin remodeling. For this reason, any nucleosome composition alterations accompanying transcriptional responses to physiological signals must occur through a DNA replication-independent pathway. HIRA is the histone chaperone primarily responsible for replicationindependent incorporation of histone variant H3.3 across gene bodies and regulatory regions. Thus, HIRA would be expected to play an important role in epigenetically regulating myocyte gene expression. The objective of this study was to determine the consequence of eliminating HIRA from mouse skeletal myocytes. At 6 weeks of age, myofibers lacking HIRA showed no pathological abnormalities; however, genes involved in transcriptional regulation were downregulated. By 6 months of age, myofibers lacking HIRA exhibited hypertrophy, sarcolemmal perforation and oxidative damage. Genes involved in muscle growth and development were upregulated, but those associated with responses to cellular stresses were downregulated. These data suggest that elimination of HIRA produces a hypertrophic response in skeletal muscle and leaves myofibers susceptible to stress-induced degeneration.

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Myogenic transcriptional activation of MyoD mediated by replication-independent histone deposition

Cited by 82 publications

References 50 publications

Histone variants: dynamic punctuation in transcription

Histone variants: dynamic punctuation in transcription

Transcription factor EKLF (KLF1) recruitment of the histone chaperone HIRA is essential for β-globin gene expression

HIRA deficiency in muscle fibers causes hypertrophy and susceptibility to oxidative stress

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