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Distinct regulatory programs for Sox9 in transcriptional regulation of the developing mammalian chondrocyte [ChIP-seq]

ABSTRACT: We compared Sox9-association at chondrocyte targets to a broad catalogue of regulatory indicators of chromatin organization and transcriptional activity to determine Sox9’s direct regulatory actions in normal developing chondrocytes. Sox9-associated regions resolve into two distinct regulatory categories. Class I regions closely associate with transcriptional start sites (TSSs). Their targets reflect general regulators of basal cell activities that Sox9 engages indirectly though a likely association with the basal transcriptional complex. In contrast, Class II regions outside of the local TSS domains highlight evolutionarily conserved, active enhancers directing expression of chondrocyte specific target genes, though DNA binding of Sox9-dimers at target sites with sub-optimal binding affinity. The level of associated chondrocyte gene expression correlates with the number of enhancer modules around the target gene and grouping into super-enhancer clusters. Comparison of Sox9 programs between neural crest and mesoderm-derived chondrocytes points to similar modes of chondrocyte specification in distinct chondrocyte lineages. These data provide the first insight into mammalian Sox family actions at the genome scale in the vivo setting. The resulting enhancer sets provide a key resource for further dissection of the regulatory programs of mammalian chondrogenesis.

ORGANISM(S): Mus musculus

PROVIDER: GSE69109 | GEO | 2015/07/01

SECONDARY ACCESSION(S): PRJNA284581

REPOSITORIES: GEO

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Distinct regulatory programs for Sox9 in transcriptional regulation of the developing mammalian chondrocyte [expression array]

Project description:We compared Sox9-association at chondrocyte targets to a broad catalogue of regulatory indicators of chromatin organization and transcriptional activity to determine Sox9’s direct regulatory actions in normal developing chondrocytes. Sox9-associated regions resolve into two distinct regulatory categories. Class I regions closely associate with transcriptional start sites (TSSs). Their targets reflect general regulators of basal cell activities that Sox9 engages indirectly though a likely association with the basal transcriptional complex. In contrast, Class II regions outside of the local TSS domains highlight evolutionarily conserved, active enhancers directing expression of chondrocyte specific target genes, though DNA binding of Sox9-dimers at target sites with sub-optimal binding affinity. The level of associated chondrocyte gene expression correlates with the number of enhancer modules around the target gene and grouping into super-enhancer clusters. Comparison of Sox9 programs between neural crest and mesoderm-derived chondrocytes points to similar modes of chondrocyte specification in distinct chondrocyte lineages. These data provide the first insight into mammalian Sox family actions at the genome scale in the vivo setting. The resulting enhancer sets provide a key resource for further dissection of the regulatory programs of mammalian chondrogenesis. Incorportation of ChIP-seq data of Sox9 and histone modification marks for chromatin status together with microrarray gene expression profiling in neonatal mice chondrocytes to uncover Sox9 regulatory system

2015-07-01 | E-GEOD-69108 | biostudies-arrayexpress

Distinct regulatory programs for Sox9 in transcriptional regulation of the developing mammalian chondrocyte [ChIP-seq]

Project description:We compared Sox9-association at chondrocyte targets to a broad catalogue of regulatory indicators of chromatin organization and transcriptional activity to determine Sox9’s direct regulatory actions in normal developing chondrocytes. Sox9-associated regions resolve into two distinct regulatory categories. Class I regions closely associate with transcriptional start sites (TSSs). Their targets reflect general regulators of basal cell activities that Sox9 engages indirectly though a likely association with the basal transcriptional complex. In contrast, Class II regions outside of the local TSS domains highlight evolutionarily conserved, active enhancers directing expression of chondrocyte specific target genes, though DNA binding of Sox9-dimers at target sites with sub-optimal binding affinity. The level of associated chondrocyte gene expression correlates with the number of enhancer modules around the target gene and grouping into super-enhancer clusters. Comparison of Sox9 programs between neural crest and mesoderm-derived chondrocytes points to similar modes of chondrocyte specification in distinct chondrocyte lineages. These data provide the first insight into mammalian Sox family actions at the genome scale in the vivo setting. The resulting enhancer sets provide a key resource for further dissection of the regulatory programs of mammalian chondrogenesis. Incorportation of ChIP-seq data of Sox9 and histone modification marks for chromatin status together with micorarray gene expression profiling in neonatal mice chondrocytes to uncover Sox9 regulatory system. Overexpression of Sox9 with a control of EGFP in human fibroblasts to identify the direct targets of Sox9 regulatory system

2015-07-01 | E-GEOD-69109 | biostudies-arrayexpress

Distinct regulatory programs for Sox9 in transcriptional regulation of the developing mammalian chondrocyte [RNA-seq]

Project description:We compared Sox9-association at chondrocyte targets to a broad catalogue of regulatory indicators of chromatin organization and transcriptional activity to determine Sox9’s direct regulatory actions in normal developing chondrocytes. Sox9-associated regions resolve into two distinct regulatory categories. Class I regions closely associate with transcriptional start sites (TSSs). Their targets reflect general regulators of basal cell activities that Sox9 engages indirectly through a likely association with the basal transcriptional complex. In contrast, Class II regions outside of the local TSS domains highlight evolutionarily conserved, active enhancers directing expression of chondrocyte specific target genes, though DNA binding of Sox9-dimers at target sites with sub-optimal binding affinity. The level of associated chondrocyte gene expression correlates with the number of enhancer modules around the target gene and grouping into super-enhancer clusters. Comparison of Sox9 programs between neural crest and mesoderm-derived chondrocytes points to similar modes of chondrocyte specification in distinct chondrocyte lineages. These data provide the first insight into mammalian Sox family actions at the genome scale in the vivo setting. The resulting enhancer sets provide a key resource for further dissection of the regulatory programs of mammalian chondrogenesis. Incorportation of ChIP-seq data of Sox9 and histone modification marks for chromatin status together with micorarray gene expression profiling in neonatal mice chondrocytes to uncover Sox9 regulatory system. Overexpression of Sox9 with a control of EGFP in human fibroblasts to identify the direct targets of Sox9 regulatory system

2015-07-01 | E-GEOD-69110 | biostudies-arrayexpress

Distinct regulatory programs for Sox9 in transcriptional regulation of the developing mammalian chondrocyte [expression array]

2015-07-01 | GSE69108 | GEO

Distinct regulatory programs for Sox9 in transcriptional regulation of the developing mammalian chondrocyte [RNA-seq]

Project description:We compared Sox9-association at chondrocyte targets to a broad catalogue of regulatory indicators of chromatin organization and transcriptional activity to determine Sox9’s direct regulatory actions in normal developing chondrocytes. Sox9-associated regions resolve into two distinct regulatory categories. Class I regions closely associate with transcriptional start sites (TSSs). Their targets reflect general regulators of basal cell activities that Sox9 engages indirectly through a likely association with the basal transcriptional complex. In contrast, Class II regions outside of the local TSS domains highlight evolutionarily conserved, active enhancers directing expression of chondrocyte specific target genes, though DNA binding of Sox9-dimers at target sites with sub-optimal binding affinity. The level of associated chondrocyte gene expression correlates with the number of enhancer modules around the target gene and grouping into super-enhancer clusters. Comparison of Sox9 programs between neural crest and mesoderm-derived chondrocytes points to similar modes of chondrocyte specification in distinct chondrocyte lineages. These data provide the first insight into mammalian Sox family actions at the genome scale in the vivo setting. The resulting enhancer sets provide a key resource for further dissection of the regulatory programs of mammalian chondrogenesis.

2015-07-01 | GSE69110 | GEO

AP-1 family members act at DNA targets in conjunction with Sox9 to promote chondrocyte hypertrophy

Project description:A comprehensive analysis of Sox9 binding profiles in developing chondrocytes identified marked enrichment of an AP-1-like motif (Ohba et al. 2015). Here, we have explored the functional interplay between Sox9 and AP-1 in mammalian chondrocyte development. Among AP-1 family members, Jun and Fosl2 were highly expressed within prehypertrophic and early hypertrophic chondrocytes. Chromatin immunoprecipitation followed by DNA sequencing (ChIP-seq) showed a striking overlap in Jun- and Sox9-bound regions throughout the chondrocyte genome, a reflection of direct binding of each factor to target motifs in shared enhancers, and physical interactions of AP-1 with Sox9. In vitro expression analysis indicates that direct co-binding of Sox9 and AP-1 at target motifs enhanced target gene expression, while protein-protein interactions suppressed AP-1- and Sox9-driven transcription. Analysis of prehypertrophic chondrocyte removal of Sox9 demonstrated Sox9 was essential for hypertrophic chondrocyte development, while in vitro and ex vivo analyses showed AP-1 promotes chondrocyte hypertrophy. Sox9 and Jun co-bound and co-activated a Col10a1 enhancer in Sox9 and AP-1 motif-dependent manners consistent with their combined action promoting hypertrophic gene expression. Together, the data support a model where AP-1-family members promote Sox9-action in the transition of chondrocytes to a terminal hypertrophic program. Intersection of ChIP-seq data from Sox9 and AP-1 factor Jun, RNA-seq data from developing rib chondrocytes and Col10a1mCherry positive hypertrophic chondrocytes in neonatal mice to uncover regulation of Sox9 by AP-1 factors during chondrocyte hypertrophy.

2016-02-29 | E-GEOD-73372 | biostudies-arrayexpress

AP-1 family members act at DNA targets in conjunction with Sox9 to promote chondrocyte hypertrophy

2016-02-29 | GSE73372 | GEO

A chondrocyte-specific Indian hedgehog enhancer activated in both skeletal development and postnatal cartilage degeneration [ChIP-seq]

Project description:Sox6-DNA interaction was profiled in the same chondrocyte population as used for our Sox9 ChIP-seq analysis (GSE69109). First, we classified Sox6 peaks into TSS-associated Class I and distally located Class II as in our previous study. Class II targets were strongly associated with genes related to skeletal tissues, whereas Class I targets were related to general cellular processes, not chondrocyte-specific activities. When we investigated the overlap of the Sox6 ChIP-seq peaks with Sox9 ChIP-seq peaks identified in our previous study, the majority of Sox9 peaks overlapped with Sox6 peaks in both Class I and Class II regions, which is in line with previous findings that Sox9 and Sox6 co-engage in gene expression for the chondrocyte program.

2020-03-31 | GSE129025 | GEO

GRNs driving cartilage and bone formation interact via averaging and synergism during cartilage maturation

Project description:Transcriptional control of any biological process occurs through the action of one to many gene regulatory networks (GRNs), but studies analyzing GRN interaction are lacking. To address this, we tested for the first time in vivo the hypothesis that two independent GRNs, which are active during formation of two discrete skeletal cell types (immature chondrocytes and osteoblasts), interact during differentiation of a third skeletal cell type (mature chondrocytes). These three cell types were isolated from the mouse embryo specifically using laser capture microdissection, and then RNA was extracted. Multiple analyses of corresponding RNA-seq data supported the hypothesis. Gene co-expression network analyses of differentially expressed genes suggested that one GRN containing the chondrogenic transcription factor Sox9 characterizes immature chondrocytes, one GRN containing the osteogenic transcription factor Runx2 characterizes osteoblasts, and both GRNs operate in mature chondrocytes. Indeed, mature chondrocytes differentially expressed fewer genes than the other cell types, consistent with the idea that overlapping actions of the immature chondrocyte and osteoblast GRNs regulate mature chondrocytes. Clustering analyses provided molecular insights into potential GRN interactions. Several genes in mature chondrocytes had expression levels that represented an averaging between levels in the immature chondrocyte and osteoblast. Interestingly, expression levels of one gene cluster, containing the hallmark mature chondrocyte genes Collagen type 10a1 and Indian hedgehog, suggested a synergistic interaction between immature chondrocyte and osteoblast GRNs. In addition to identifying novel genes expressed in mature chondrocytes, these results outline a novel in vivo experimental system through which to understand GRN organization and interaction.

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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

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