Chromatin profiling identifies chondrocyte-specific Sox9 enhancers important for skeletal development Article Swipe
Sachi Ichiyama‐Kobayashi
,
Kenji Hata
,
Kanta Wakamori
,
Yoshifumi Takahata
,
Tomohiko Murakami
,
Hitomi Yamanaka
,
Hiroshi Takano
,
Ryoji Yao
,
Narikazu Uzawa
,
Riko Nishimura
·
YOU?
·
· 2024
· Open Access
·
· DOI: https://doi.org/10.1172/jci.insight.175486
YOU?
·
· 2024
· Open Access
·
· DOI: https://doi.org/10.1172/jci.insight.175486
The transcription factor SRY-related HMG box 9 (Sox9) is essential for chondrogenesis. Mutations in and around SOX9 cause campomelic dysplasia (CD) characterized by skeletal malformations. Although the function of Sox9 in this context is well studied, the mechanisms that regulate Sox9 expression in chondrocytes remain to be elucidated. Here, we have used genome-wide profiling to identify 2 Sox9 enhancers located in a proximal breakpoint cluster responsible for CD. Enhancer activity of E308 (located 308 kb 5' upstream) and E160 (located 160 kb 5' upstream) correlated with Sox9 expression levels, and both enhancers showed a synergistic effect in vitro. While single deletions in mice had no apparent effect, simultaneous deletion of both E308 and E160 caused a dwarf phenotype, concomitant with a reduction of Sox9 expression in chondrocytes. Moreover, bone morphogenetic protein 2-dependent chondrocyte differentiation of limb bud mesenchymal cells was severely attenuated in E308/E160 deletion mice. Finally, we found that an open chromatin region upstream of the Sox9 gene was reorganized in the E308/E160 deletion mice to partially compensate for the loss of E308 and E160. In conclusion, our findings reveal a mechanism of Sox9 gene regulation in chondrocytes that might aid in our understanding of the pathophysiology of skeletal disorders.
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Metadata
- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.1172/jci.insight.175486
- http://insight.jci.org/articles/view/175486/files/pdf
- OA Status
- gold
- Cited By
- 6
- References
- 62
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4399476483
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
-
https://openalex.org/W4399476483Canonical identifier for this work in OpenAlex
- DOI
-
https://doi.org/10.1172/jci.insight.175486Digital Object Identifier
- Title
-
Chromatin profiling identifies chondrocyte-specific Sox9 enhancers important for skeletal developmentWork title
- Type
-
articleOpenAlex work type
- Language
-
enPrimary language
- Publication year
-
2024Year of publication
- Publication date
-
2024-06-09Full publication date if available
- Authors
-
Sachi Ichiyama‐Kobayashi, Kenji Hata, Kanta Wakamori, Yoshifumi Takahata, Tomohiko Murakami, Hitomi Yamanaka, Hiroshi Takano, Ryoji Yao, Narikazu Uzawa, Riko NishimuraList of authors in order
- Landing page
-
https://doi.org/10.1172/jci.insight.175486Publisher landing page
- PDF URL
-
https://insight.jci.org/articles/view/175486/files/pdfDirect link to full text PDF
- Open access
-
YesWhether a free full text is available
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-
goldOpen access status per OpenAlex
- OA URL
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https://insight.jci.org/articles/view/175486/files/pdfDirect OA link when available
- Concepts
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Enhancer, Chromatin, SOX9, Computational biology, Profiling (computer programming), Chondrocyte, Biology, Cell biology, Transcription factor, Genetics, Computer science, Gene, In vitro, Operating systemTop concepts (fields/topics) attached by OpenAlex
- Cited by
-
6Total citation count in OpenAlex
- Citations by year (recent)
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2025: 3, 2024: 3Per-year citation counts (last 5 years)
- References (count)
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62Number of works referenced by this work
- Related works (count)
-
10Other works algorithmically related by OpenAlex
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| abstract_inverted_index.effect | 95 |
| abstract_inverted_index.factor | 2 |
| abstract_inverted_index.region | 153 |
| abstract_inverted_index.remain | 44 |
| abstract_inverted_index.reveal | 180 |
| abstract_inverted_index.showed | 92 |
| abstract_inverted_index.single | 99 |
| abstract_inverted_index.vitro. | 97 |
| abstract_inverted_index.cluster | 64 |
| abstract_inverted_index.context | 32 |
| abstract_inverted_index.effect, | 106 |
| abstract_inverted_index.levels, | 88 |
| abstract_inverted_index.located | 59 |
| abstract_inverted_index.protein | 130 |
| abstract_inverted_index.(located | 72, 79 |
| abstract_inverted_index.Although | 25 |
| abstract_inverted_index.Enhancer | 68 |
| abstract_inverted_index.Finally, | 146 |
| abstract_inverted_index.activity | 69 |
| abstract_inverted_index.apparent | 105 |
| abstract_inverted_index.deletion | 108, 144, 164 |
| abstract_inverted_index.findings | 179 |
| abstract_inverted_index.function | 27 |
| abstract_inverted_index.identify | 55 |
| abstract_inverted_index.proximal | 62 |
| abstract_inverted_index.regulate | 39 |
| abstract_inverted_index.severely | 140 |
| abstract_inverted_index.skeletal | 23, 199 |
| abstract_inverted_index.studied, | 35 |
| abstract_inverted_index.upstream | 154 |
| abstract_inverted_index.E308/E160 | 143, 163 |
| abstract_inverted_index.Moreover, | 127 |
| abstract_inverted_index.Mutations | 12 |
| abstract_inverted_index.chromatin | 152 |
| abstract_inverted_index.deletions | 100 |
| abstract_inverted_index.dysplasia | 19 |
| abstract_inverted_index.enhancers | 58, 91 |
| abstract_inverted_index.essential | 9 |
| abstract_inverted_index.mechanism | 182 |
| abstract_inverted_index.partially | 167 |
| abstract_inverted_index.profiling | 53 |
| abstract_inverted_index.reduction | 121 |
| abstract_inverted_index.upstream) | 76, 83 |
| abstract_inverted_index.attenuated | 141 |
| abstract_inverted_index.breakpoint | 63 |
| abstract_inverted_index.campomelic | 18 |
| abstract_inverted_index.compensate | 168 |
| abstract_inverted_index.correlated | 84 |
| abstract_inverted_index.disorders. | 200 |
| abstract_inverted_index.expression | 41, 87, 124 |
| abstract_inverted_index.mechanisms | 37 |
| abstract_inverted_index.phenotype, | 117 |
| abstract_inverted_index.regulation | 186 |
| abstract_inverted_index.2-dependent | 131 |
| abstract_inverted_index.SRY-related | 3 |
| abstract_inverted_index.chondrocyte | 132 |
| abstract_inverted_index.conclusion, | 177 |
| abstract_inverted_index.concomitant | 118 |
| abstract_inverted_index.elucidated. | 47 |
| abstract_inverted_index.genome-wide | 52 |
| abstract_inverted_index.mesenchymal | 137 |
| abstract_inverted_index.reorganized | 160 |
| abstract_inverted_index.responsible | 65 |
| abstract_inverted_index.synergistic | 94 |
| abstract_inverted_index.chondrocytes | 43, 188 |
| abstract_inverted_index.simultaneous | 107 |
| abstract_inverted_index.characterized | 21 |
| abstract_inverted_index.chondrocytes. | 126 |
| abstract_inverted_index.morphogenetic | 129 |
| abstract_inverted_index.transcription | 1 |
| abstract_inverted_index.understanding | 194 |
| abstract_inverted_index.malformations. | 24 |
| abstract_inverted_index.chondrogenesis. | 11 |
| abstract_inverted_index.differentiation | 133 |
| abstract_inverted_index.pathophysiology | 197 |
| cited_by_percentile_year.max | 97 |
| cited_by_percentile_year.min | 96 |
| corresponding_author_ids | https://openalex.org/A5028445962, https://openalex.org/A5087356195 |
| countries_distinct_count | 2 |
| institutions_distinct_count | 10 |
| citation_normalized_percentile.value | 0.88975895 |
| citation_normalized_percentile.is_in_top_1_percent | False |
| citation_normalized_percentile.is_in_top_10_percent | True |