Sarah J. Bray

The paper investigates how transcription factor handover between Notch and Broad regulates the temporal progression of gene expression through dynamic hub formation.

This study shows SMARCA4 mutations in T-ALL lead to chemotherapy resistance by altering chromatin remodeling at AP-1 regulatory regions, reducing stress response genes.

The paper investigates the role of core promoters in gene expression specificity by testing their interaction with enhancers in Drosophila.

The paper shows that morphological differences influence Notch-mediated lateral inhibition, biasing cells toward signal-sending or receiving roles during neuroblast selection.

This study identifies SPARC as a mediator of tumour-stroma communication by regulating endosomal Delta and Notch signalling in a Drosophila cancer model.

This study identifies that both sequence-specific DNA binding and disordered protein domains are required for pioneer-factor chromatin occupancy, with mitotic retention relying only on DNA binding.

This study identifies E(spl)m4 as an inhibitor of Traf4 signaling in Drosophila, preventing JNK activation and cell delamination without affecting Adherens Junctions.

The paper shows Notch signaling forms transcription hubs that regulate gene expression by correlating hub dynamics with transcription profiles.

The paper investigates changes in CSL transcription complex behavior under Notch active conditions using single molecule microscopy, finding increased binding and exploratory behavior.

The paper reveals that Notch transcription hubs form dynamically in nuclei and confer memory, with only a third progressing to transcription, influenced by a second signal.

The paper uses an optogenetic approach to control Notch signaling and shows that the {Phi}W{Phi}P motif sequesters CSL in the cytoplasm, preventing target gene activation until NICD is released.

The paper shows that gastrulation movements in Drosophila increase Notch-responsive enhancer activity, suggesting mechanical forces influence transcription levels.

The paper investigates how loss of epithelial polarity and Notch signaling interact in Drosophila neoplastic growth, showing specific transcriptional dependencies and novel factors involved.

The paper shows that adherens junctions enhance Notch pathway activation during Drosophila embryonic cellularization by facilitating membrane contact formation.

The paper shows that the Delta C2 domain β1-2 loop is essential for phospholipid binding and robust Notch signaling in Drosophila.

The paper shows Notch signaling regulates ommatidial rotation in Drosophila by upregulating argos, an EGFR ligand, through direct transcriptional control in R4 photoreceptors.

The paper shows how enhancers decode Notch signaling by altering transcription burst duration and requiring priming by transcription factors for sustained activity.

The paper shows that the SWI/SNF chromatin remodeling complex is essential for Notch-responsive enhancer accessibility by facilitating nucleosome turnover and H3.3 incorporation.

The paper shows that the Mi-2/NuRD complex suppresses Notch signaling in Drosophila neural stem cell progeny, preventing excessive stem cell proliferation and hyperplasia.

The paper shows that Drosophila muscle progenitors maintain a satellite-like state by switching RNA-isoforms of zfh1, which protects them from differentiation.