A scalable, high-throughput neural development platform identifies shared impact of ASD genes on cell fate and differentiation
Wang, X.; Lalli, M. A.; Thopte, U.; Buxbaum, J.
Show abstract
BackgroundDeleterious mutations in hundreds of genes confer high risk for neurodevelopmental disorders (NDDs), posing significant challenges for therapeutic development. Identifying convergent pathways shared across NDD genes could reveal high-impact therapeutic targets. MethodsTo identity convergent pathways in NDD genes, we optimized Perturb-seq, a method combining CRISPR perturbation with single-cell RNA sequencing (scRNA-seq), and applied structural topic modeling (STM) to simultaneously assess impact on cell fate and developmental stage. We then studied a subset of autism spectrum disorder (ASD) genes implicated in regulation of gene expression using these improved molecular and analytical approaches. ResultsResults from targeting 60 high-confidence ASD risk genes revealed significant effects on neural development. As expected, ASD risk genes impacted both progenitor fate and/or neuronal differentiation. Using STM, we could identify latent topics jointly capturing cell types, cell fate, and differentiation stages. Repression of ASD risk genes led to changes in topic proportions and effects of four genes (DEAF1, KMT2A, MED13L, and MYT1L) were validated in an independent dataset. ConclusionsOur optimized Perturb-seq method, combined with a novel analytical approach, provides a powerful, cost-effective framework for uncovering convergent mechanisms among genes involved in complex neurodevelopmental processes. Application of these methods advanced understanding of the impact of ASD mutations on multiple dimensions of neural development, and provides a framework for a broader examination of the function of NDD risk genes.
Matching journals
The top 10 journals account for 50% of the predicted probability mass.
Similar papers in this journal
- Neuron-specific transcriptomic signatures indicate neuroinflammation and altered neuronal activity in ASD temporal cortex 96%
- Diencephalic and Neuropeptidergic Dysfunction in Zebrafish with Autism Risk Mutations 95%
- A Kalirin Missense Mutation Enhances Dendritic RhoA Signaling and Leads to Regression of Cortical Dendritic Arbors Across Development 94%
Similar papers in this journal
- Alterations in retrotransposition, synaptic connectivity, and myelination implicated by transcriptomic changes following maternal immune activation in non-human primates 96%
- Loss of Zmiz1 in mice leads to impaired cortical development and autistic-like behaviors 94%
- Gene expression in patient-derived neural progenitors implicates WNT5A signaling in the etiology of schizophrenia 93%
Similar papers in this journal
- Systematic analysis of genetic and phenotypic characteristics reveals antisense oligonucleotide therapy potential for one-third of neurodevelopmental disorders 93%
- Cord blood DNA methylome in newborns later diagnosed with autism spectrum disorder reflects early dysregulation of neurodevelopmental and X-linked genes 93%
- Improved analysis of CRISPR fitness screens and reduced off-target effects with the BAGEL2 gene essentiality classifier 92%
Similar papers in this journal
- Genome-wide, integrative analysis implicates circular RNA dysregulation in autism and the corresponding circular RNA-microRNA-mRNA regulatory axes 94%
- Co-expression enrichment analysis at the single-cell level reveals convergent defects in neural progenitor cells and their cell-type transitions in neurodevelopmental disorders 93%
- Autism spectrum disorder risk genes have convergent effects on transcription and neuronal firing patterns in primary neurons 93%
Similar papers in this journal
- An antisense oligonucleotide-based strategy to ameliorate cognitive dysfunction in the 22q11.2 Deletion Syndrome 94%
- Heterozygosity for neurodevelopmental disorder-associated TRIO variants yields distinct deficits in behavior, neuronal development, and synaptic transmission in mice. 93%
- Discovery and characterization of LNCSOX17 as an essential regulator in human endoderm formation 92%
"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.