Eyal Ben‐David

The paper identifies immune cell type-specific gene expression regulated by tandem repeats using multi-omics data from large cohorts.

The paper investigates how interdependent protein interactions evolve by studying toxin-antidote elements, finding that toxins and antidotes can arise simultaneously through the duplication of a regulatory module.

The paper maps chromatin accessibility and genetic variation in immune cells, showing how integrating cell-type-specific data improves disease risk understanding.

The paper analyzes whole-animal single-cell transcriptomes of nematodes to reveal stable neuronal identities but divergent signaling pathways across species.

The paper presents a single-cell multi-omics atlas of human development and uses deep learning to analyze regulatory DNA motifs and their impact on chromatin accessibility and gene expression.

The paper analyzes two extremophilic algae to understand their iron management strategies, identifying novel iron-uptake proteins and adaptive mechanisms that enable survival in low-iron environments.

The paper investigates how selfish toxin-antidote elements evade silencing in C. tropicalis by showing maternal mRNA licenses zygotic expression through counteracting piRNAs.

The paper identifies chromosome 1 in Schmidtea mediterranea as a sex-primed autosome through genomic analysis showing restricted recombination and sex-specific gene expression.

The paper maps eQTLs at cellular resolution in C. elegans using single-cell RNA sequencing, revealing cell-type-specific and single-cell-specific eQTL effects.

The paper identifies toxin-antidote elements in Caenorhabditis species, showing they cause developmental delay and are subject to balancing selection.

This paper introduces ceX-QTL, a method for fast genetic mapping of complex traits in C. elegans using bulk selection on millions of individuals, and demonstrates its application in identifying drug resistance, gene expression, and fitness loci.

The paper shows that different mutation classes affect distinct pathways in neuropsychiatric disorders, explaining genetic convergence and specific gene expression patterns across ID, ASD, and SCZ.