Proper Gcn5 histone acetyltransferase expression is required for normal anteroposterior patterning of the mouse skeleton

Lin, Wenchu; Zhang, Zhijing; Chen, Chih Hsin; Behringer, Richard R.; Dent, Sharon Y.R.

doi:10.1111/j.1440-169x.2008.01041.x

Cited by 27 publications

(27 citation statements)

References 60 publications

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“…Of interest, work in Drosophila has associated histone acetylation to temporal-spatial expression of the Hox gene locus (48,49). The evolutionary predecessor of PCAF in Drosophila is GCN5, and indeed GCN5 has been linked to Hox gene regulation in murine skeletal development (50). We therefore speculate that the novel mechanistic observation of recruitment of PCAF to the FOXP3 core promoter through KLF-PRE may represent an evolutionarily conserved mechanism of FOXP3 gene regulation.…”

Section: Antagonism Of Prc2 Function By a Klf-pcaf Pathway Marks The mentioning

confidence: 87%

Polycomb Antagonizes p300/CREB-binding Protein-associated Factor to Silence FOXP3 in a Kruppel-like Factor-dependent Manner

Xiong

Khanna

Grzenda

et al. 2012

Journal of Biological Chemistry

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Background: Epigenetic regulation of the T regulatory cell transcriptional program remains unclear. Results: Without KLF10, Polycomb permanently silences FOXP3, the master transcription factor of T regulatory cells. Conclusion: Chromatin remodeling events mediated by KLF10 and Polycomb regulate FOXP3 through a Polycomb response element. Significance: Polycomb and KLFs may direct a heritable, broadly applicable regulatory circuit within T cell development.

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Section: Antagonism Of Prc2 Function By a Klf-pcaf Pathway Marks The mentioning

confidence: 87%

Polycomb Antagonizes p300/CREB-binding Protein-associated Factor to Silence FOXP3 in a Kruppel-like Factor-dependent Manner

Xiong

Khanna

Grzenda

et al. 2012

Journal of Biological Chemistry

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“…Gcn5 floxed mice were used as described previously (Chen et al, 2012; Lin et al, 2008). Mice were backcrossed onto the C57/BL6 genetic background for 7 generations.…”

Section: Methodsmentioning

confidence: 99%

The Lysine Acetyltransferase GCN5 Is Required for iNKT Cell Development through EGR2 Acetylation

et al. 2017

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Summary The development of CD1d-restricted invariant NKT (iNKT) cells, a population that is critical for both innate and adaptive immunity, is regulated by multiple transcription factors, but the molecular mechanisms underlying how the transcriptional activation of these factors are regulated during iNKT development remain largely unknown. We found that the histone acetyltransferase GCN5 is essential for iNKT cell development during the maturation stage. GCN5 deficiency blocked iNKT cell development in a cell-intrinsic manner. At the molecular level, GCN5 is a specific lysine acetyltransferase of EGR2, a transcription factor required for iNKT cell development. GCN5-mediated acetylation positively regulated EGR2 transcriptional activity, and both genetic and pharmacological GCN5 suppression specifically inhibited the transcription of EGR2 target genes in iNKT cells, including Runx1, PLZF, IL-2Rb, and T-bet. Therefore, our study revealed GCN5-mediated EGR2 acetylation as a molecular mechanism that regulates iNKT development.

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“…Combination of a hypomorphic allele of Gcn5 with a deletion allele in mice to reduce expression below 50% causes homeotic transformations in the skeleton, as well as exencephaly [40,41]. Mice homozygous for a catalytically inactive allele of Gcn5 die in mid-gestation with severe neural tube closure defects [42].…”

Section: Developmental Functions Of Gcn5 and Pcafmentioning

confidence: 99%

Functions of SAGA in development and disease

2014

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Precise regulation of gene expression programs during embryo development requires cooperation between transcriptional factors and histone-modifying enzymes, such as the Gcn5 histone acetyltransferase. Gcn5 functions within a multi-subunit complex, called SAGA, that is recruited to specific genes through interactions with sequence-specific DNA-binding proteins to aid in gene activation. Although the transcriptional programs regulated by SAGA in embryos are not well defined, deletion of either Gcn5 or USP22, the catalytic subunit of a deubiquitinase module in SAGA, leads to early embryonic lethality. Here, we review the known functions of Gcn5, USP22 and associated proteins during development and discuss how these functions might be related to human disease states, including cancer and neurodegenerative diseases.

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Proper Gcn5 histone acetyltransferase expression is required for normal anteroposterior patterning of the mouse skeleton

Cited by 27 publications

References 60 publications

Polycomb Antagonizes p300/CREB-binding Protein-associated Factor to Silence FOXP3 in a Kruppel-like Factor-dependent Manner

Polycomb Antagonizes p300/CREB-binding Protein-associated Factor to Silence FOXP3 in a Kruppel-like Factor-dependent Manner

The Lysine Acetyltransferase GCN5 Is Required for iNKT Cell Development through EGR2 Acetylation

Functions of SAGA in development and disease

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