Abstract:
:Development of the craniofacial structures requires the precise differentiation of cranial neural crest cells into osteoblasts or chondrocytes. Here, we explore the epigenetic and non-epigenetic mechanisms that are required for the development of craniofacial chondrocytes. We previously demonstrated that the acetyltransferase activity of the highly conserved acetyltransferase GCN5, or KAT2A, is required for murine craniofacial development. We show that Gcn5 is required cell autonomously in the cranial neural crest. Moreover, GCN5 is required for chondrocyte development following the arrival of the cranial neural crest within the pharyngeal arches. Using a combination of in vivo and in vitro inhibition of GCN5 acetyltransferase activity, we demonstrate that GCN5 is a potent activator of chondrocyte maturation, acting to control chondrocyte maturation and size increase during pre-hypertrophic maturation to hypertrophic chondrocytes. Rather than acting as an epigenetic regulator of histone H3K9 acetylation, our findings suggest GCN5 primarily acts as a non-histone acetyltransferase to regulate chondrocyte development. Here, we investigate the contribution of GCN5 acetylation to the activity of the mTORC1 pathway. Our findings indicate that GCN5 acetylation is required for activation of this pathway, either via direct activation of mTORC1 or through indirect mechanisms. We also investigate one possibility of how mTORC1 activity is regulated through RAPTOR acetylation, which is hypothesized to enhance mTORC1 downstream phosphorylation. This study contributes to our understanding of the specificity of acetyltransferases, and the cell type specific roles in which these enzymes function.
journal_name
Dev Bioljournal_title
Developmental biologyauthors
Pezoa SA,Artinger KB,Niswander LAdoi
10.1016/j.ydbio.2020.05.006subject
Has Abstractpub_date
2020-08-01 00:00:00pages
24-34issue
1eissn
0012-1606issn
1095-564Xpii
S0012-1606(20)30151-2journal_volume
464pub_type
杂志文章abstract::Connexin 43 (Cx43) knockout mice and transgenic mice (CMV43) overexpressing the Cx43 gap junction gene exhibit heart defects involving the conotruncus and right ventricle. Based on the heart phenotype and Cx43 gene and transgene expression pattern, we previously proposed that the heart defects may reflect a role for g...
journal_title:Developmental biology
pub_type: 杂志文章
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journal_title:Developmental biology
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journal_title:Developmental biology
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journal_title:Developmental biology
pub_type: 杂志文章
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journal_title:Developmental biology
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journal_title:Developmental biology
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journal_title:Developmental biology
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abstract::Notch signaling has a fundamental role in stem cell maintenance and in cell fate choice in the intestine of different species. Canonically, Notch signaling represses the expression of transcription factors of the achaete-scute like (ASCL) or atonal related protein (ARP) families. Identifying the ARP/ASCL genes express...
journal_title:Developmental biology
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更新日期:2013-04-15 00:00:00
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journal_title:Developmental biology
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journal_title:Developmental biology
pub_type: 杂志文章
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journal_title:Developmental biology
pub_type: 杂志文章
doi:10.1016/j.ydbio.2006.01.003
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journal_title:Developmental biology
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更新日期:2010-09-15 00:00:00
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journal_title:Developmental biology
pub_type: 杂志文章
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journal_title:Developmental biology
pub_type: 杂志文章
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journal_title:Developmental biology
pub_type: 杂志文章
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journal_title:Developmental biology
pub_type: 杂志文章
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更新日期:2001-11-15 00:00:00
abstract::The structure of the three polypeptide chains of the laminin subunits and the number of glycosylation sites in each polypeptide chain were determined using peptide mapping by high-performance liquid chromatography. Analysis of the [35S]methionine-labeled underglycosylated laminin isolated from tunicamycin (TM)-treated...
journal_title:Developmental biology
pub_type: 杂志文章
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journal_title:Developmental biology
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journal_title:Developmental biology
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journal_title:Developmental biology
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