Project description:Chondrocytes undergo a series of sequential differentiation steps which result in the formation of a unique hierarchical columnar structure including proliferating, pre-hypertrophic and hypertrophic chondrocytes. Pre-hypertrophic chondrocytes, which exist in the transitional stage between proliferating and hypertrophic chondrocytes, are a rare cell population in the growth plate but critical for endochondral bone development. However, the molecular basis of pre-hypertrophic chondrocytes largely remains elusive. The purpose of this study is to identify novel marker gene and uncover regulatory mechanism of marker gene expression.
Project description:The transcription factor Sox9 (Sry-Related HMG-Box gene 9) is essential in chondrogenesis. The expression Sox9 is regulated by 1.5Mb long range genomic region in temporospatial manner and genome translocation or deletion which affect Sox9 expression cause campomelic dysplasia (CD), characterized by skeletal malformations. Although functional mechanism of Sox9 are well studied so far, regulatory mechanism of Sox9 expression and its related enhancer in chondrocytes are largely remains to be elucidated. The purpose of this study is to identify Sox9 enhancers in chondrocytes
Project description:The transcription factor Sox9 (Sry-Related HMG-Box gene 9) is essential in chondrogenesis. The expression Sox9 is regulated by 1.5Mb long range genomic region in temporospatial manner and genome translocation or deletion which affect Sox9 expression cause campomelic dysplasia (CD), characterized by skeletal malformations. Although functional mechanism of Sox9 are well studied so far, regulatory mechanism of Sox9 expression and its related enhancer in chondrocytes are largely remains to be elucidated. The purpose of this study is to identify Sox9 enhancers in chondrocytes
Project description:The transcription factor Sox9 (Sry-Related HMG-Box gene 9) is essential in chondrogenesis. The expression Sox9 is regulated by 1.5Mb long range genomic region in temporospatial manner and genome translocation or deletion which affect Sox9 expression cause campomelic dysplasia (CD), characterized by skeletal malformations. Although functional mechanism of Sox9 are well studied so far, regulatory mechanism of Sox9 expression and its related enhancer in chondrocytes are largely remains to be elucidated. The purpose of this study is to identify Sox9 enhancers in chondrocytes
Project description:Chromatin accessibility change of chondrocytes in vitro remains unclear. We performed ATAC-seq of P1,P3, and P6 cells in vitro to explore chromatin accessibility change.