Barak A. Cohen

The paper evaluates differential expression methods for metatranscriptomes, identifies limitations, and proposes improvements using real datasets from gnotobiotic mice and clinical studies.

This paper introduces DAF-seq, a method for single-molecule and single-cell chromatin fiber sequencing, enabling precise analysis of protein occupancy and chromatin accessibility.

This study identifies functional non-coding variants associated with orofacial cleft by combining GWAS, reporter assays, and stem cell modeling.

The paper introduces a long-range MPRA assay to measure enhancer-promoter interactions and finds that enhancer strength and transcription factor binding influence long-range activity.

The paper uses active learning to improve models of enhancer and silencer activities in mouse retina, achieving better discrimination between functionally distinct TF binding sites.

The paper performs a deep mutational scan of CRX variants to classify clinical variants and reveals biochemical properties of the transcriptional effector domain.

The paper develops MPIRE to assess insulator activity across the genome, finding that insulators function in specific genomic contexts and depend on transcription factor binding.

The paper examines how different pathogenic variants in the CRX gene affect cis-regulatory elements in photoreceptors, showing overlapping enhancer effects and distinct silencer impacts.

The paper shows CRX binding sites can act as enhancers or silencers based on sequence context, with negative homotypic interactions causing silencing and positive interactions or other TFBSs overcoming this.

The paper develops a method to assess the functional effects of non-coding elements in specific cell types in vivo using a Cre-dependent MPRA approach.

The paper shows that stochastic fluctuations in Prrx1 transcription factor activity contribute to cell-to-cell variability in Hedgehog signaling response in NIH3T3-CG cells.

This study maps postzygotic mutations across tissues and lifespan, showing their functional variation and selection pressures, suggesting multiple dynamic genomes per individual.

The paper introduces scMPRA, a single-cell assay to measure cis-regulatory activity across cell types, showing it detects cell-type specific effects of genetic variants in retinas.

The paper introduces a quantitative metric to measure pioneer activity of transcription factors and finds HNF4A has stronger in vivo pioneer activity than FOXA1.

The paper tests the regulatory activity of human LTR18A transposable elements and finds they have lost activity over time due to mutations in AP-1 and C/EBP motifs.

The paper introduces SARGENT, a method to measure gene expression noise and mean expression across the genome, finding correlations between noise and histone modifications, and linking extrinsic noise to cell sub-states.

The paper identifies three design principles of acidic transcriptional activation domains through experimental analysis and develops a predictor to identify these domains in the human proteome.

The paper tests the Pioneer Factor Hypothesis by expressing FoxA1 and Hnf4a in K562 cells, finding no functional distinction between the two TFs and proposing an alternative model based on binding affinity and genomic context.

The paper measures core promoter activities across different genomic locations and finds that their intrinsic strengths are preserved, supporting the classical model of gene regulation.

The paper identifies sequence features that distinguish enhancers from silencers in mouse photoreceptors by analyzing TF motifs and information content.

The paper measures how gene promoters and chromatin environments independently affect expression noise across different chromosomal locations.

This study identifies CELF6 mRNA targets using CLIP-Seq and shows CELF6 represses synaptic gene translation by reducing RNA abundance through UGU-rich motifs, extending its known role beyond splicing.

The paper uses MPRA libraries to analyze cis-regulatory grammar in mouse ESCs, finding that synthetic and genomic elements share binding site quality as a key factor, but genomic activity is better explained by binding site affinity and spacing.

This study uses a deep mutational scan to analyze the sequence features of an acidic activation domain, finding that acidic residues help expose hydrophobic motifs and that activity increases under amino acid starvation.