David Yao

The paper uses an image-based CRISPR screen to show splicing regulates HP1α condensates through RNA-chromatin interactions, affecting heterochromatin organization and stress response genes.

The paper identifies ZMAT3 and CDKN1A as key hubs in the p53 tumor suppression network through integrative multiomic analyses in a mouse model.

The paper shows that enhancer-promoter communication scales with genomic distance in a gene-specific manner, independent of 3D contact frequency or chromatin state.

The paper develops HT-recruit to measure transcriptional effector function across contexts and identifies context-dependent effectors for CRISPR-based transcription control.

ENCODE-rE2G, a classifier trained on K562 CRISPR perturbations, maps 13,455,443 enhancer-gene interactions across 352 biosamples, matching or exceeding prior models on CRISPR, eQTL, and GWAS benchmarks.

The paper uses CRISPR screens in human forebrain assembloids to identify NDD genes involved in interneuron generation and migration, revealing novel roles for the ER in migration.

Splice Editing uses CRISPR-mediated trans-splicing to correct large RNA segments in human cells, enabling efficient and specific RNA and protein correction without DNA mutagenesis.

The paper reports 109 non-coding CRISPR screens analyzing 13.3Mb of the genome, identifies CRE-gene links, and provides guidelines and tools for screening non-coding regulatory elements.

The paper develops HT-recruit, a high-throughput assay to identify transcriptional effectors in human proteins, finding repressor function correlates with evolutionary age and discovering new activator domains.

The paper identifies off-target effects in CRISPR-Cas9 screens for non-coding elements and shows that strict filtering with specificity scores improves the identification of essential regulatory regions.

The paper identifies rare genetic variants that cause large disruptions to exon recognition, using a new assay called MFASS, and finds most of these variants are not in canonical splice sites.