Josh Tycko

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 presents a workflow using machine learning to optimize protein function and reduce immunogenicity in cell and gene therapies.

The paper evaluates how base editor design features affect editing efficiency and mutation patterns in mammalian cells, identifying DivA-BE as the most effective variant.

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

This paper introduces an IFFL-based CRISPR-Cas system to reduce gene expression variability, demonstrating improved dosage control for RAI1 in a mouse model.

This study shows that CRISPRa systems can cause cytotoxicity, limiting their use in research and genetic screens.

The paper predicts and designs transcriptional repressor domains using mutational scans and a deep learning model called TENet, identifying functional variants and enabling synthetic design.

The paper measures how combinations of transcriptional activators and repressors affect gene expression and uses this to create a tunable synthetic transcription factor.

The paper identifies and characterizes viral transcriptional effector domains from coronaviruses and herpesviruses using high-throughput assays and perturbations.

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 systematically maps and characterizes transcriptional effector domains in human chromatin regulators and transcription factors, identifying new activation and repression domains and their functional features.

This study develops a population genetic and epidemiological model to assess the potential of CRISPR gene drives for schistosomiasis control, showing they could maintain disease reduction when combined with chemotherapy.

The paper introduces a method to profile off-target specificity of CRISPR enzymes using ssDNA mapping, applicable to both catalytically dead and active Cas9 variants.

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.

This paper uses HiChIP to map enhancer-promoter interactions in primary human cells, linking disease-associated DNA variants to their target genes.