Specific ZNF274 binding interference at SNORD116 activates the maternal transcripts in Prader-Willi syndrome neurons Article Swipe
Maéva Langouët
,
Dea Gorka
,
Clarisse Orniacki
,
Clémence Dupont-Thibert
,
Michael Chung
,
Heather R. Glatt-Deeley
,
Noélle D. Germain
,
Leann Crandall
,
Justin Cotney
,
Christopher Stoddard
,
Marc Lalande
,
Stormy J. Chamberlain
·
YOU?
·
· 2020
· Open Access
·
· DOI: https://doi.org/10.1093/hmg/ddaa210
YOU?
·
· 2020
· Open Access
·
· DOI: https://doi.org/10.1093/hmg/ddaa210
Prader-Willi syndrome (PWS) is characterized by neonatal hypotonia, developmental delay and hyperphagia/obesity. This disorder is caused by the absence of paternally expressed gene products from chromosome 15q11–q13. We previously demonstrated that knocking out ZNF274, a Kruppel-associated box-A-domain zinc finger protein capable of recruiting epigenetic machinery to deposit the H3K9me3 repressive histone modification, can activate expression from the normally silent maternal allele of SNORD116 in neurons derived from PWS induced pluripotent stem cells (iPSCs). However, ZNF274 has many other targets in the genome in addition to SNORD116. Depleting ZNF274 will surely affect the expression of other important genes and disrupt other pathways. Here, we used CRISPR/Cas9 to delete ZNF274 binding sites at the SNORD116 locus to determine whether activation of the maternal copy of SNORD116 could be achieved without altering ZNF274 protein levels. We obtained similar activation of gene expression from the normally silenced maternal allele in neurons derived from PWS iPSCs, compared with ZNF274 knockout, demonstrating that ZNF274 is directly involved in the repression of SNORD116. These results suggest that interfering with ZNF274 binding at the maternal SNORD116 locus is a potential therapeutic strategy for PWS.
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- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.1093/hmg/ddaa210
- https://academic.oup.com/hmg/article-pdf/29/19/3285/34544967/ddaa210.pdf
- OA Status
- bronze
- Cited By
- 17
- References
- 62
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W3087884128
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W3087884128Canonical identifier for this work in OpenAlex
- DOI
-
https://doi.org/10.1093/hmg/ddaa210Digital Object Identifier
- Title
-
Specific ZNF274 binding interference at SNORD116 activates the maternal transcripts in Prader-Willi syndrome neuronsWork title
- Type
-
articleOpenAlex work type
- Language
-
enPrimary language
- Publication year
-
2020Year of publication
- Publication date
-
2020-09-18Full publication date if available
- Authors
-
Maéva Langouët, Dea Gorka, Clarisse Orniacki, Clémence Dupont-Thibert, Michael Chung, Heather R. Glatt-Deeley, Noélle D. Germain, Leann Crandall, Justin Cotney, Christopher Stoddard, Marc Lalande, Stormy J. ChamberlainList of authors in order
- Landing page
-
https://doi.org/10.1093/hmg/ddaa210Publisher landing page
- PDF URL
-
https://academic.oup.com/hmg/article-pdf/29/19/3285/34544967/ddaa210.pdfDirect link to full text PDF
- Open access
-
YesWhether a free full text is available
- OA status
-
bronzeOpen access status per OpenAlex
- OA URL
-
https://academic.oup.com/hmg/article-pdf/29/19/3285/34544967/ddaa210.pdfDirect OA link when available
- Concepts
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Biology, Interference (communication), RNA interference, Genetics, Cell biology, Gene, RNA, Electrical engineering, Engineering, Channel (broadcasting)Top concepts (fields/topics) attached by OpenAlex
- Cited by
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17Total citation count in OpenAlex
- Citations by year (recent)
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2024: 5, 2023: 4, 2022: 5, 2021: 3Per-year citation counts (last 5 years)
- References (count)
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62Number of works referenced by this work
- Related works (count)
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10Other works algorithmically related by OpenAlex
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| abstract_inverted_index.expressed | 22 |
| abstract_inverted_index.important | 96 |
| abstract_inverted_index.knockout, | 155 |
| abstract_inverted_index.machinery | 45 |
| abstract_inverted_index.pathways. | 101 |
| abstract_inverted_index.potential | 182 |
| abstract_inverted_index.activation | 118, 136 |
| abstract_inverted_index.chromosome | 26 |
| abstract_inverted_index.epigenetic | 44 |
| abstract_inverted_index.expression | 55, 93, 139 |
| abstract_inverted_index.hypotonia, | 8 |
| abstract_inverted_index.paternally | 21 |
| abstract_inverted_index.previously | 29 |
| abstract_inverted_index.recruiting | 43 |
| abstract_inverted_index.repression | 164 |
| abstract_inverted_index.repressive | 50 |
| abstract_inverted_index.CRISPR/Cas9 | 105 |
| abstract_inverted_index.interfering | 171 |
| abstract_inverted_index.pluripotent | 70 |
| abstract_inverted_index.therapeutic | 183 |
| abstract_inverted_index.15q11–q13. | 27 |
| abstract_inverted_index.Prader-Willi | 1 |
| abstract_inverted_index.box-A-domain | 37 |
| abstract_inverted_index.demonstrated | 30 |
| abstract_inverted_index.characterized | 5 |
| abstract_inverted_index.demonstrating | 156 |
| abstract_inverted_index.developmental | 9 |
| abstract_inverted_index.modification, | 52 |
| abstract_inverted_index.Kruppel-associated | 36 |
| abstract_inverted_index.hyperphagia/obesity. | 12 |
| cited_by_percentile_year.max | 98 |
| cited_by_percentile_year.min | 95 |
| corresponding_author_ids | https://openalex.org/A5022238852 |
| countries_distinct_count | 1 |
| institutions_distinct_count | 12 |
| corresponding_institution_ids | https://openalex.org/I140172145 |
| sustainable_development_goals[0].id | https://metadata.un.org/sdg/3 |
| sustainable_development_goals[0].score | 0.8299999833106995 |
| sustainable_development_goals[0].display_name | Good health and well-being |
| citation_normalized_percentile.value | 0.88122162 |
| citation_normalized_percentile.is_in_top_1_percent | False |
| citation_normalized_percentile.is_in_top_10_percent | False |