MLL1 promotes myogenesis by epigenetically regulating <i>Myf5</i>

Cai, Shaohui; Zhu, Qi; Guo, Cilin; Yuan, Renqiang; Zhang, Xumeng; Nie, Yaping; Chen, Luxi; Fāng, Yīng; Chen, Keren; Zhang, Junyan; Mo, Delin

doi:10.1111/cpr.12744

Cited by 19 publications

(20 citation statements)

References 42 publications

(85 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…HMT recruitment at Myf5 underlies the importance of PAX7 expression for activation and proliferation of MuSCs. In the same context, MLL1 KO also displays diminution of Myf5 gene and protein expression in proliferating primary myoblasts and C2C12 cells [31,43]. These effects observed in proliferating myoblasts are consistent with the fact that Pax7 expression needs to be maintained during the transition from quiescence to proliferation and during the proliferation.…”

Section: Epigenetic Histone Modifications Contributing To the Prolifesupporting

confidence: 71%

Epigenetic regulation of satellite cell fate during skeletal muscle regeneration

et al. 2021

View full text Add to dashboard Cite

In response to muscle injury, muscle stem cells integrate environmental cues in the damaged tissue to mediate regeneration. These environmental cues are tightly regulated to ensure expansion of muscle stem cell population to repair the damaged myofibers while allowing repopulation of the stem cell niche. These changes in muscle stem cell fate result from changes in gene expression that occur in response to cell signaling from the muscle environment.Integration of signals from the muscle environment leads to changes in gene expression through epigenetic mechanisms. Such mechanisms, including post-translational modification of chromatin and nucleosome repositioning, act to make specific gene loci more, or less, accessible to the transcriptional machinery. In youth, the muscle environment is ideally structured to allow for coordinated signaling that mediates efficient regeneration. Both age and disease alter the muscle environment such that the signaling pathways that shape the healthy muscle stem cell epigenome are altered. Altered epigenome reduces the efficiency of cell fate transitions required for muscle repair and contributes to muscle pathology. However, the reversible nature of epigenetic changes holds out potential for restoring cell fate potential to improve muscle repair in myopathies.In this review, we will describe the current knowledge of the mechanisms allowing muscle stem cell fate transitions during regeneration and how it is altered in muscle disease. In addition, we provide some examples of how epigenetics could be harnessed therapeutically to improve regeneration in various muscle pathologies.

show abstract

Section: Epigenetic Histone Modifications Contributing To the Prolifesupporting

confidence: 71%

Epigenetic regulation of satellite cell fate during skeletal muscle regeneration

et al. 2021

View full text Add to dashboard Cite

show abstract

“…In line with this report, we found that the accumulation of PARP1 inversely correlates with that of H3K4me3 at KvDMR1 and myogenin promoter. Since MLL1 is highly expressed in muscle cells and seems to regulate both proliferation and differentiation 84 , the possibility of its functional interaction with PARP1 during myogenesis will deserve further investigation. Although it is conceivable that the decreased levels of H3K4me3, by promoting a repressive chromatin environment, are responsible for the PARP1-dependent exclusion of MyoD from its targets, we still cannot exclude that the accumulation of H3K4me3 is a result of transcriptional activation consequent to MyoD binding.…”

Section: Discussionmentioning

confidence: 99%

Poly(ADP-ribose) Polymerase 1 (PARP1) restrains MyoD-dependent gene expression during muscle differentiation

Matteini

Andresini

Petrai

et al. 2020

Sci Rep

View full text Add to dashboard Cite

The myogenic factor MyoD regulates skeletal muscle differentiation by interacting with a variety of chromatin-modifying complexes. Although MyoD can induce and maintain chromatin accessibility at its target genes, its binding and trans-activation ability can be limited by some types of not fully characterized epigenetic constraints. In this work we analysed the role of PARP1 in regulating MyoD-dependent gene expression. PARP1 is a chromatin-associated enzyme, playing a well recognized role in DNA repair and that is implicated in transcriptional regulation. PARP1 affects gene expression through multiple mechanisms, often involving the Poly(ADP-ribosyl)ation of chromatin proteins. In line with PARP1 down-regulation during differentiation, we observed that PARP1 depletion boosts the up-regulation of MyoD targets, such as p57, myogenin, Mef2C and p21, while its re-expression reverts this effect. We also found that PARP1 interacts with some MyoD-binding regions and that its presence, independently of the enzymatic activity, interferes with MyoD recruitment and gene induction. We finally suggest a relationship between the binding of PARP1 and the loss of the activating histone modification H3K4me3 at MyoD-binding regions. This work highlights not only a novel player in the epigenetic control of myogenesis, but also a repressive and catalytic-independent mechanisms by which PARP1 regulates transcription.

show abstract

“…Available evidence suggests that downregulation of cyclin D1 in C2C12 cells leads to G1-phase arrest. [31][32][33] Therefore, S6K1 regulates cell cycle through promoting Myf5 and cyclin D1 expression.…”

Section: Discussionmentioning

confidence: 99%

High mobility group box 2 regulates skeletal muscle development through ribosomal protein S6 kinase 1

et al. 2020

Self Cite

View full text Add to dashboard Cite

HMGB2, a DNA‐binding protein, highly expresses during embryogenesis and plays an important role in development of some organs and tissues. However, it remains to be further investigated weather HMGB2 influences muscle development. In this work, we identified HMGB2 as an essential factor in myogenesis. Compared to wild type (WT) mice, body weights of systemic hmgb2 homozygous knockout (hmgb2−/−) mice especially males were reduced. Diameter and cross‐section area of tibialis anterior (TA) muscle fibers as well as expression of Myogenin and MyHC were all decreased in hmgb2−/− mice. CTX injury model revealed that HMGB2 was required for satellite cell proliferation and muscle regeneration. Moreover, HMGB2 interacted with S6K1 and regulated the kinase activity of S6K1 during cell proliferation. Knockdown and inactivation of S6K1 in C2C12 cells both resulted in impaired proliferation and differentiation. Furthermore, expression of cyclin D1 and Myf5 were both decreased when HMGB2 or S6K1 were knocked down and kinase activity of S6K1 was inhibited. These results indicate that HMGB2 is required for skeletal muscle development and regeneration, and HMGB2 maintains proliferation of myoblasts through regulating kinase activity of S6K1.

show abstract

MLL1 promotes myogenesis by epigenetically regulating Myf5

Cited by 19 publications

References 42 publications

Epigenetic regulation of satellite cell fate during skeletal muscle regeneration

Epigenetic regulation of satellite cell fate during skeletal muscle regeneration

Poly(ADP-ribose) Polymerase 1 (PARP1) restrains MyoD-dependent gene expression during muscle differentiation

High mobility group box 2 regulates skeletal muscle development through ribosomal protein S6 kinase 1

Contact Info

Product

Resources

About