High resolution mapping of transcriptional repression reveals complex and interdependent mechanisms that underpin rapid transitions between transcriptional states.

First comprehensive genetic analysis of a Myt1 family protein reveals that neurogenesis requires direct repression of non-neuronal identities by the Myt1 family protein through MuvB co-repressor complex.

GLI3 represses Hedgehog target gene expression by regulating histone modifications at a subset of tissue-specific GLI-bound enhancers.

An integrative genome-wide approach supports a direct and collaborative role of ETS and AP-1 transcription factors in maintaining endothelial cell-specific and anti-inflammatory gene expression programs.

Experimental results in Drosophila support a model in which gene expression is fundamentally controlled by morphogens tuning the same transcription parameter for genes that are expressed in highly diverse patterns.

X-ray crystallography reveals the structural framework for understanding the function of mammalian transcriptional repression in the cellular circadian clock.

Tuned protein–protein interaction affinity optimizes the repressive function of the ETS family transcription factor Yan in order to contribute specificity and robustness to cell fate specification in the developing Drosophila eye.

Uncovering the mechanisms by which the transcription factor NRSF contributes to the development of epilepsy reveals that the regulation of gene expression by transcription factors in the brain is more finely-tuned than previously thought.

The transcription factor ztf-11 promotes neuronal differentiation by repressing other cell fates in the nematode worm C. elegans.

Analysis of the atypical tryptophan biosynthetic operon of Chlamydia trachomatis revealed the simultaneous regulation of transcriptional initiation and termination by an iron-dependent repressor, expanding known regulatory mechanisms of this pathway.