Naama Barkai

The paper shows that Med15's activator-binding domains are necessary but not sufficient for UAS recruitment, and its disordered C-terminus is critical for directing genome targeting.

The paper investigates how human transcription factors bind specific DNA sites in yeast, finding that disordered regions influence binding selectivity beyond DNA motifs.

The paper identifies Pex9's role in regulating TORC2 during oxidative stress in yeast, revealing a non-canonical signaling pathway independent of Yap1 and Skn7.

The paper analyzes the overlap between transcription factor binding and regulatory targets in yeast, finding that low overlap is due to weakly bound sites.

This study identifies design principles of transcription factor intrinsically disordered regions that enhance binding affinity and search time for target DNA.

The paper introduces pMPBA, a method to analyze peptide-DNA binding in yeast, revealing determinants both within and outside predicted DNA binding domains.

The paper challenges the model of transcription factor binding cooperativity by showing limited effects of motif combinatorics in yeast using a novel massively parallel binding assay.

This study identifies Yet3 as a protein that recruits sterol biosynthesis enzymes to ER contact sites, enabling on-demand sterol production and influencing organellar structure and function.

The paper uses a histone exchange sensor to study variant-specific dynamics of histone incorporation and exchange in mouse embryonic stem cells, revealing variant-specific associations with transcription and Polycomb binding.

The paper uses a histone exchange sensor to show Rtt109 promotes H3 replacement ahead of the replication fork in budding yeast, independent of H3K56 acetylation.

The paper examines how duplicated transcription factors in budding yeast evolve binding preferences, finding that most divergence occurs outside DNA binding domains and that new targets are acquired by the least conserved paralog.

The paper investigates how morphogen gradients, specifically the Dorsal protein gradient in Drosophila embryos, generate graded responses through transcriptional and translational mechanisms.

The paper investigates how gene transcription limits protein production and cell growth by analyzing the effects of transcriptional feedback and its impact on cell size and division time.

The paper profiles gene expression in related yeast species across hundreds of conditions to distinguish transcriptional regulation from expression level variation, finding that promoter strength changes drive divergence without altering network positioning.

The paper shows that transcription factor binding to replicated DNA increases with DNA dosage, while RNA polymerase II binding remains stable during S phase in budding yeast.

The paper shows that gene duplication in budding yeast allows stress regulators to function cooperatively, reducing noise while maintaining environmental responsiveness.

The paper shows that diffusion-based morphogen shuttling and dynamic nuclear readout refine pattern formation in Drosophila embryos.

The paper quantifies how G1 cyclins affect cell cycle phase durations in yeast through transcriptome-wide analysis under genetic and stress perturbations.

The paper shows that repressor-decay timers are more robust than activator-relay timers in Drosophila neuroblast lineages, supporting a repressor-decay mechanism for temporal patterning.

The paper describes a yeast hybrid with increased growth rate and biomass yield under various conditions, but identifies genetic perturbations and regulatory disruptions associated with heterosis.