Polycomb Ezh1 maintains murine muscle stem cell quiescence through non-canonical regulation of Notch signaling

Feng, Xuesong; Wang, A Hongjun; Juan, Aster H.; Ko, Kyung Dae; Jiang, Kan; Riparini, Giulia; Ciuffoli, Veronica; Kaba, Aissah; Lopez, Christopher D.; Naz, Faiza; Jarník, Michal; Aliberti, Elizabeth; Hu, Shenyuan; Segalés, Jessica; Khateb, Mamduh; Acevedo-Luna, Natalia; Randazzo, Davide; Cheung, Tom H.; Muñoz‐Cánoves, Pura; Dell’Orso, Stefania; Sartorelli, Vittorio

doi:10.1016/j.devcel.2023.04.005

Cited by 5 publications

(1 citation statement)

References 141 publications

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“…With repeated muscle injuries, the muscle stem cell pool is progressively depleted, leading to compromised muscle regeneration capabilities. EZH1 plays a crucial role in sustaining the expression of Notch signaling pathway genes in SCs, preventing their premature activation [ 114 ].…”

Section: The Role Of Epigenetic In Skeletal Muscle Atrophymentioning

confidence: 99%

Epigenetic control of skeletal muscle atrophy

Liang,

Xu,

et al. 2024

Cell Mol Biol Lett

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Skeletal muscular atrophy is a complex disease involving a large number of gene expression regulatory networks and various biological processes. Despite extensive research on this topic, its underlying mechanisms remain elusive, and effective therapeutic approaches are yet to be established. Recent studies have shown that epigenetics play an important role in regulating skeletal muscle atrophy, influencing the expression of numerous genes associated with this condition through the addition or removal of certain chemical modifications at the molecular level. This review article comprehensively summarizes the different types of modifications to DNA, histones, RNA, and their known regulators. We also discuss how epigenetic modifications change during the process of skeletal muscle atrophy, the molecular mechanisms by which epigenetic regulatory proteins control skeletal muscle atrophy, and assess their translational potential. The role of epigenetics on muscle stem cells is also highlighted. In addition, we propose that alternative splicing interacts with epigenetic mechanisms to regulate skeletal muscle mass, offering a novel perspective that enhances our understanding of epigenetic inheritance’s role and the regulatory network governing skeletal muscle atrophy. Collectively, advancements in the understanding of epigenetic mechanisms provide invaluable insights into the study of skeletal muscle atrophy. Moreover, this knowledge paves the way for identifying new avenues for the development of more effective therapeutic strategies and pharmaceutical interventions.

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Section: The Role Of Epigenetic In Skeletal Muscle Atrophymentioning

confidence: 99%

Epigenetic control of skeletal muscle atrophy

Liang,

Xu,

et al. 2024

Cell Mol Biol Lett

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Epigenetic integration of signaling from the regenerative environment

Geara,

Dilworth

2024

Current Topics in Developmental Biology

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PRC2-EZH1 contributes to circadian gene expression by orchestrating chromatin states and RNA polymerase II complex stability

Liu,

Nadeef,

Serag

et al. 2024

EMBO J

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Circadian rhythmicity of gene expression is a conserved feature of cell physiology. This involves fine-tuning between transcriptional and post-transcriptional mechanisms and strongly depends on the metabolic state of the cell. Together these processes guarantee an adaptive plasticity of tissue-specific genetic programs. However, it is unclear how the epigenome and RNA Pol II rhythmicity are integrated. Here we show that the PcG protein EZH1 has a gateway bridging function in postmitotic skeletal muscle cells. On the one hand, the circadian clock master regulator BMAL1 directly controls oscillatory behavior and periodic assembly of core components of the PRC2–EZH1 complex. On the other hand, EZH1 is essential for circadian gene expression at alternate Zeitgeber times, through stabilization of RNA Polymerase II preinitiation complexes, thereby controlling nascent transcription. Collectively, our data show that PRC2–EZH1 regulates circadian transcription both negatively and positively by modulating chromatin states and basal transcription complex stability.

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Polycomb Ezh1 maintains murine muscle stem cell quiescence through non-canonical regulation of Notch signaling

Cited by 5 publications

References 141 publications

Epigenetic control of skeletal muscle atrophy

Epigenetic control of skeletal muscle atrophy

Epigenetic integration of signaling from the regenerative environment

PRC2-EZH1 contributes to circadian gene expression by orchestrating chromatin states and RNA polymerase II complex stability

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