期刊
CELL REPORTS
卷 12, 期 2, 页码 229-243出版社
CELL PRESS
DOI: 10.1016/j.celrep.2015.06.013
关键词
-
类别
资金
- NIH [DK056246]
- JSPS [23689079, 26713054, 15K15732, 24240069, 26221311]
- Takeda Science Foundation Research Grant
- Graduate Program for Leaders in Life Innovation
- Core-to-Core Program A Advanced Research Networks
- Grants-in-Aid for Scientific Research [15K15732, 26713054, 23689079, 26221311] Funding Source: KAKEN
Sox9 encodes an essential transcriptional regulator of chondrocyte specification and differentiation. When Sox9 nuclear activity was compared with markers of chromatin organization and transcriptional activity in primary chondrocytes, we identified two distinct categories of target association. Class I sites cluster around the transcriptional start sites of highly expressed genes with no chondrocyte-specific signature. Here, Sox9 association reflects protein-protein association with basal transcriptional components. Class II sites highlight evolutionarily conserved active enhancers that direct chondrocyte-related gene activity through the direct binding of Sox9 dimer complexes to DNA. Sox9 binds through sites with sub-optimal binding affinity; the number and grouping of enhancers into super-enhancer clusters likely determines the levels of target gene expression. Interestingly, comparison of Sox9 action in distinct chondrocyte lineages points to similar regulatory strategies. In addition to providing insights into Sox family action, our comprehensive identification of the chondrocyte regulatory genome will facilitate the study of skeletal development and human disease.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据