Developmental convergence and divergence in human stem cell models of autism spectrum disorder Article Swipe
Aaron Gordon
,
Se‐Jin Yoon
,
Lucy Bicks
,
Jacqueline M. Martín
,
Greta Pintacuda
,
Stephanie Arteaga
,
Brie Wamsley
,
Qiuyu Guo
,
Lubayna Elahi
,
Ricardo Dolmetsch
,
Jonathan A. Bernstein
,
Ruth O’Hara
,
Joachim Hallmayer
,
Kasper Lage
,
Sergiu P. Pașca
,
Daniel H. Geschwind
·
YOU?
·
· 2024
· Open Access
·
· DOI: https://doi.org/10.1101/2024.04.01.587492
YOU?
·
· 2024
· Open Access
·
· DOI: https://doi.org/10.1101/2024.04.01.587492
Two decades of genetic studies in autism spectrum disorder (ASD) have identified over a hundred genes harboring rare risk mutations. Despite this substantial heterogeneity, transcriptomic and epigenetic analyses have identified convergent patterns of dysregulation across ASD post-mortem brain tissue. To identify shared and distinct mutational mechanisms, we assembled the largest hiPS cell patient cohort to date, consisting of 70 hiPS cell lines after stringent quality control representing 8 ASD-associated mutations, idiopathic ASD, and 20 lines from non-affected controls. We used these hiPS lines to generate human cortical organoids (hCO), profiling by RNAseq at four distinct timepoints up to 100 days of in vitro differentiation. Early timepoints harbored the largest mutation-specific changes, but different genetic forms converged on shared transcriptional changes as development progressed. We identified a shared RNA and protein interaction network, which was enriched in ASD risk genes and predicted to drive the observed down-stream changes in gene expression. CRISPR-Cas9 screening of these candidate transcriptional regulators in induced human neural progenitors validated their downstream molecular convergent effects. These data illustrate how genetic risk can propagate via transcriptional regulation to impact convergently dysregulated pathways, providing new insight into the convergent impact of ASD genetic risk on human neurodevelopment.
Related Topics
Concepts
Biology
Epigenetics
Autism spectrum disorder
Autism
Transcriptome
Genetics
Gene
Genetic heterogeneity
Gene regulatory network
Computational biology
Gene expression
Phenotype
Medicine
Psychiatry
Metadata
- Type
- preprint
- Language
- en
- Landing Page
- https://doi.org/10.1101/2024.04.01.587492
- https://www.biorxiv.org/content/biorxiv/early/2024/04/02/2024.04.01.587492.full.pdf
- OA Status
- green
- Cited By
- 9
- References
- 151
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4393434680
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W4393434680Canonical identifier for this work in OpenAlex
- DOI
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https://doi.org/10.1101/2024.04.01.587492Digital Object Identifier
- Title
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Developmental convergence and divergence in human stem cell models of autism spectrum disorderWork title
- Type
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preprintOpenAlex work type
- Language
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enPrimary language
- Publication year
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2024Year of publication
- Publication date
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2024-04-02Full publication date if available
- Authors
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Aaron Gordon, Se‐Jin Yoon, Lucy Bicks, Jacqueline M. Martín, Greta Pintacuda, Stephanie Arteaga, Brie Wamsley, Qiuyu Guo, Lubayna Elahi, Ricardo Dolmetsch, Jonathan A. Bernstein, Ruth O’Hara, Joachim Hallmayer, Kasper Lage, Sergiu P. Pașca, Daniel H. GeschwindList of authors in order
- Landing page
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https://doi.org/10.1101/2024.04.01.587492Publisher landing page
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https://www.biorxiv.org/content/biorxiv/early/2024/04/02/2024.04.01.587492.full.pdfDirect link to full text PDF
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YesWhether a free full text is available
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greenOpen access status per OpenAlex
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https://www.biorxiv.org/content/biorxiv/early/2024/04/02/2024.04.01.587492.full.pdfDirect OA link when available
- Concepts
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Biology, Epigenetics, Autism spectrum disorder, Autism, Transcriptome, Genetics, Gene, Genetic heterogeneity, Gene regulatory network, Computational biology, Gene expression, Phenotype, Medicine, PsychiatryTop concepts (fields/topics) attached by OpenAlex
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9Total citation count in OpenAlex
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2025: 5, 2024: 4Per-year citation counts (last 5 years)
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10Other works algorithmically related by OpenAlex
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| abstract_inverted_index.shared | 42, 118, 127 |
| abstract_inverted_index.Despite | 21 |
| abstract_inverted_index.changes | 120, 147 |
| abstract_inverted_index.control | 66 |
| abstract_inverted_index.decades | 2 |
| abstract_inverted_index.genetic | 4, 114, 173, 194 |
| abstract_inverted_index.hundred | 15 |
| abstract_inverted_index.induced | 159 |
| abstract_inverted_index.insight | 187 |
| abstract_inverted_index.largest | 50, 109 |
| abstract_inverted_index.patient | 53 |
| abstract_inverted_index.protein | 130 |
| abstract_inverted_index.quality | 65 |
| abstract_inverted_index.studies | 5 |
| abstract_inverted_index.tissue. | 39 |
| abstract_inverted_index.Abstract | 0 |
| abstract_inverted_index.analyses | 28 |
| abstract_inverted_index.changes, | 111 |
| abstract_inverted_index.cortical | 87 |
| abstract_inverted_index.disorder | 9 |
| abstract_inverted_index.distinct | 44, 95 |
| abstract_inverted_index.effects. | 168 |
| abstract_inverted_index.enriched | 135 |
| abstract_inverted_index.generate | 85 |
| abstract_inverted_index.harbored | 107 |
| abstract_inverted_index.identify | 41 |
| abstract_inverted_index.network, | 132 |
| abstract_inverted_index.observed | 145 |
| abstract_inverted_index.patterns | 32 |
| abstract_inverted_index.spectrum | 8 |
| abstract_inverted_index.assembled | 48 |
| abstract_inverted_index.candidate | 155 |
| abstract_inverted_index.controls. | 78 |
| abstract_inverted_index.converged | 116 |
| abstract_inverted_index.different | 113 |
| abstract_inverted_index.harboring | 17 |
| abstract_inverted_index.molecular | 166 |
| abstract_inverted_index.organoids | 88 |
| abstract_inverted_index.pathways, | 184 |
| abstract_inverted_index.predicted | 141 |
| abstract_inverted_index.profiling | 90 |
| abstract_inverted_index.propagate | 176 |
| abstract_inverted_index.providing | 185 |
| abstract_inverted_index.screening | 152 |
| abstract_inverted_index.stringent | 64 |
| abstract_inverted_index.validated | 163 |
| abstract_inverted_index.consisting | 57 |
| abstract_inverted_index.convergent | 31, 167, 190 |
| abstract_inverted_index.downstream | 165 |
| abstract_inverted_index.epigenetic | 27 |
| abstract_inverted_index.identified | 12, 30, 125 |
| abstract_inverted_index.idiopathic | 71 |
| abstract_inverted_index.illustrate | 171 |
| abstract_inverted_index.mutational | 45 |
| abstract_inverted_index.mutations, | 70 |
| abstract_inverted_index.mutations. | 20 |
| abstract_inverted_index.regulation | 179 |
| abstract_inverted_index.regulators | 157 |
| abstract_inverted_index.timepoints | 96, 106 |
| abstract_inverted_index.CRISPR-Cas9 | 151 |
| abstract_inverted_index.development | 122 |
| abstract_inverted_index.down-stream | 146 |
| abstract_inverted_index.expression. | 150 |
| abstract_inverted_index.interaction | 131 |
| abstract_inverted_index.mechanisms, | 46 |
| abstract_inverted_index.post-mortem | 37 |
| abstract_inverted_index.progenitors | 162 |
| abstract_inverted_index.progressed. | 123 |
| abstract_inverted_index.substantial | 23 |
| abstract_inverted_index.convergently | 182 |
| abstract_inverted_index.dysregulated | 183 |
| abstract_inverted_index.non-affected | 77 |
| abstract_inverted_index.representing | 67 |
| abstract_inverted_index.dysregulation | 34 |
| abstract_inverted_index.ASD-associated | 69 |
| abstract_inverted_index.heterogeneity, | 24 |
| abstract_inverted_index.transcriptomic | 25 |
| abstract_inverted_index.transcriptional | 119, 156, 178 |
| abstract_inverted_index.differentiation. | 104 |
| abstract_inverted_index.mutation-specific | 110 |
| abstract_inverted_index.neurodevelopment. | 198 |
| cited_by_percentile_year.max | 98 |
| cited_by_percentile_year.min | 97 |
| countries_distinct_count | 1 |
| institutions_distinct_count | 16 |
| sustainable_development_goals[0].id | https://metadata.un.org/sdg/3 |
| sustainable_development_goals[0].score | 0.49000000953674316 |
| sustainable_development_goals[0].display_name | Good health and well-being |
| citation_normalized_percentile.value | 0.90866218 |
| citation_normalized_percentile.is_in_top_1_percent | False |
| citation_normalized_percentile.is_in_top_10_percent | True |