GCN5 acetylation is required for craniofacial chondrocyte maturation

Pezoa, Sofia A.; Artinger, Kristin; Niswander, Lee

doi:10.1016/j.ydbio.2020.05.006

Cited by 9 publications

(3 citation statements)

References 64 publications

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“…GCN5 acts through activation of mTORC1 or indirect mechanisms rather than as an epigenetic regulator of H3K9ac. GCN5 is not required for H3K9ac at Acan enhancers specific for pre-hypertrophic chondrocytes (Pezoa et al, 2020). These results suggest the complexity of GCN5 in regulation of skeletal development and distinct mode of actions in different species.…”

Section: Writers Regulating Chondrocyte Fatementioning

confidence: 83%

Histone Modifications and Chondrocyte Fate: Regulation and Therapeutic Implications

Wan

Zhang

Yao

et al. 2021

Front. Cell Dev. Biol.

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The involvement of histone modifications in cartilage development, pathology and regeneration is becoming increasingly evident. Understanding the molecular mechanisms and consequences of histone modification enzymes in cartilage development, homeostasis and pathology provides fundamental and precise perspectives to interpret the biological behavior of chondrocytes during skeletal development and the pathogenesis of various cartilage related diseases. Candidate molecules or drugs that target histone modifying proteins have shown promising therapeutic potential in the treatment of cartilage lesions associated with joint degeneration and other chondropathies. In this review, we summarized the advances in the understanding of histone modifications in the regulation of chondrocyte fate, cartilage development and pathology, particularly the molecular writers, erasers and readers involved. In addition, we have highlighted recent studies on the use of small molecules and drugs to manipulate histone signals to regulate chondrocyte functions or treat cartilage lesions, in particular osteoarthritis (OA), and discussed their potential therapeutic benefits and limitations in preventing articular cartilage degeneration or promoting its repair or regeneration.

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Section: Writers Regulating Chondrocyte Fatementioning

confidence: 83%

Histone Modifications and Chondrocyte Fate: Regulation and Therapeutic Implications

Wan

Zhang

Yao

et al. 2021

Front. Cell Dev. Biol.

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“…Chromatin remodeling disorders associated with craniofacial malformation (Dong et al, 2023;Pezoa et al, 2020;Sen et al, 2018) (Continues) Investigating the cell type-specific nature of specialized dual roles of DNMT3B and its accessory function is needed to determine its functions in non-neural crest tissues or whether its function in neural crest development is cell autonomous.…”

Section: Ncc Formation and Differentiationmentioning

confidence: 99%

“…Like KAT6A, KAT6B activates osteogenic differentiation by interacting with RUNX2 through the C‐terminal serine/methionine domains (Pelletier et al, 2002). Two other HATs, KAT2A (also known as GCN5) and KAT2B (also known as PCAF) control craniofacial chondrocyte differentiation and maturation programs through direct histone acetylation of H3K9 as well as through non‐HAT activity and indirect control of the mTORC1 pathway (Dong et al, 2023; Pezoa et al, 2020; Sen et al, 2018).…”

Section: Dual Activating and Repressing Functions Of Histone Modifica...mentioning

confidence: 99%

Epigenetic regulation of craniofacial development and disease

Shull,

Artinger

2023

Birth Defects Research

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BackgroundThe formation of the craniofacial complex relies on proper neural crest development. The gene regulatory networks (GRNs) and signaling pathways orchestrating this process have been extensively studied. These GRNs and signaling cascades are tightly regulated as alterations to any stage of neural crest development can lead to common congenital birth defects, including multiple syndromes affecting facial morphology as well as nonsyndromic facial defects, such as cleft lip with or without cleft palate. Epigenetic factors add a hierarchy to the regulation of transcriptional networks and influence the spatiotemporal activation or repression of specific gene regulatory cascades; however less is known about their exact mechanisms in controlling precise gene regulation.AimsIn this review, we discuss the role of epigenetic factors during neural crest development, specifically during craniofacial development and how compromised activities of these regulators contribute to congenital defects that affect the craniofacial complex.

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