Zeba Wunderlich

The paper investigates the evolutionary origins of shadow enhancers in fly and mouse genomes, finding that duplication and transposable element co-option contribute to their formation.

The paper uses ATAC-seq data and TF footprinting tools to identify novel cis-regulatory elements in Drosophila embryos, finding that many TF binding sites lie outside known enhancers.

The paper identifies immune-specific enhancers in Drosophila using STARR-seq and ATAC-seq, revealing distinct TFBS motifs associated with different aspects of the immune response.

This study shows that NF-κB activation and enhancer features lead to transcriptional heterogeneity in Drosophila immune cells.

This study compares NF-κB activity in two jellyfish species, showing differences in transcriptional activation and subcellular localization.

The paper investigates how multiple promoters in the Drosophila knirps locus integrate enhancer inputs, revealing promoter-specific enhancer preferences and the role of redundancy in gene expression.

The paper investigates how transgenic reporters affect enhancer activity and endogenous gene expression in Drosophila embryos, finding inhibitory effects and competition for transcription factors.

The paper infers mechanistic gene networks from single-cell data and shows they outperform neural networks in predicting gene dynamics and knockout effects.

The paper shows that a mutation in a minimal enhancer of Drosophila eve stripe 2 is buffered by flanking sequences in extended enhancer constructs, but not in the endogenous context.

The paper shows shadow enhancers reduce transcription factor noise by separating TF inputs, leading to more stable gene expression across temperature changes.

The paper investigates the HbP2 enhancer in Drosophila, showing that cooperative binding of Bcd is insufficient to explain its sharp expression pattern, and identifies other factors like pioneer factors and histone modifiers as key contributors.

The paper compares anterior-posterior patterning gene expression across five Drosophila species to identify evolutionary changes in developmental programs.

The paper shows that Caudal counter-represses Hunchback to enable even-skipped stripe 2 expression in Drosophila embryos, challenging the traditional view of Hunchback as a direct activator.

SiteOut is an online tool that designs DNA sequences without binding sites for specified factors, allowing for precise control over regulatory DNA sequences.

The paper shows that Hunchback regulates two enhancers with opposite activities to produce the same gene expression pattern in Drosophila embryos.

This study shows that rearranging enhancers in the even-skipped locus of Drosophila embryos affects gene expression levels but not their position.