Edda G. Schulz

The paper identifies H3K9me3 accumulation at the Xist promoter as a transcription-dependent mechanism that influences random XCI choice in female cells.

The paper shows that antisense transcription can create expression memory through promoter repression in mouse embryonic stem cells, with memory capacity increasing during differentiation.

The paper uses CRISPR screens to identify transcription factors regulating Xist expression and their interactions with cis-regulatory elements during X-chromosome inactivation.

CasTuner enables analog tuning of endogenous gene expression using CRISPR/Cas systems and a degron domain, showing dose-dependent repression and application in studying gene dosage effects.

This study shows that human blastoids and pluripotent stem cells can enter a dormant state via mTOR inhibition, with distinct temporal dynamics compared to mice.

This study identifies GATA transcription factors as essential for initiating Xist upregulation and X-chromosome inactivation in mouse embryos through direct activation of a distal enhancer.

The paper identifies distal and proximal cis-regulatory elements that respond to X-chromosomal dosage and developmental state to regulate Xist expression during XCI in mouse embryonic stem cells.

The paper uses allele-specific single-cell RNA-sequencing to study Xist upregulation and gene silencing during X-chromosome inactivation in mouse embryonic stem cells, identifying Nanog downregulation as a trigger and genetic variation's role in XCI.

The paper identifies X-chromosomal genes, including Klhl13, that drive sex differences in murine embryonic stem cells by affecting pluripotency and differentiation.

The paper predicts Xist-induced gene silencing kinetics using a Random Forest model based on epigenetic and genomic features, identifying key factors like distance to Xist and promoter pre-marking.

The paper identifies a symmetric toggle switch as the mechanism for random Xist up-regulation during X-chromosome inactivation in mammals.