Édith Heard

The paper investigates the role of CTCF and cohesin in X-inactivation escapee domains and finds that these domains are self-sustaining chromatin compartments independent of CTCF and cohesin.

The paper shows that aged female CD8 memory T cells exhibit erosion of Xi transcriptional fidelity, linked to immune activation and clonal expansion, with similar findings in humans.

The paper identifies NuRD's role in tethering pioneer factors like SOX2 to transcription sites, enhancing ERK-dependent gene activation and maintaining cell identity.

The paper identifies a female-specific neurodevelopmental disorder caused by biallelic CIZ1 loss-of-function variants, which disrupt X-chromosome inactivation maintenance.

The paper presents a mouse pangenome with 17 strains, resolving structural complexity and improving RNA-Seq analysis by identifying non-reference genes and VNTR polymorphisms.

The paper identifies an X-Y translocation in Four-Core Genotypes mice that increases Tlr7 expression and affects genetic interpretation.

This study shows Xist RNA modulates X-chromosome inactivation beyond early development, reversibly silencing escapee genes and altering topological domain structures in mouse embryos.

This study perturbs LINE-1 elements in mouse embryonic stem cells to show their cis-regulatory impact on gene expression, with 1,024 genes misregulated upon activation and 81 upon repression.

The paper examines how XIST regulatory networks evolve in primates, showing extensive diversification and the role of transposons and enhancers in different species.

The paper uses multi-omics analysis to compare malignant and normal uveal melanocytes, identifying genomic instability and a BAP1 promoter deletion as key features of uveal melanoma.

The paper shows that RNA polymerase II depletion from the inactive X chromosome is due to reduced chromatin binding, not biophysical compartmentalization.

The paper inverts a topological domain and shows it causes limited gene expression changes but affects inter-domain communication, particularly in Xist expression.

This study shows that SPEN is essential for Xist upregulation during X chromosome inactivation initiation in female mouse ESCs by silencing Tsix.

The paper investigates random monoallelic expression (RME) in F1 hybrid mouse cells before and after differentiation, revealing gene-specific, epigenetically regulated modes of allelic expression.

The paper tracks H3K27me3 and H4K20me1 dynamics during XCI and finds they accumulate concurrently but have distinct genomic distributions, with H4K20me1 possibly contributing to chromatin compaction.

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.

This study shows that SmcHD1 prevents TAD formation on the inactive X chromosome by altering chromatin structure and epigenetic marks.

This study investigates the role of Polycomb recruitment in Xist-mediated X chromosome silencing in mouse ES cells, finding that silencing can occur independently of Polycomb complexes.

This paper introduces a normalization method for Hi-C data that accounts for copy number variations, improving downstream analysis of genome organization.

The paper investigates X-linked gene reactivation in mouse inner cell mass by analyzing epigenetic marks and transcription factors, finding differential reactivation speeds and mechanisms.

This study identifies gene expression differences in NMR brain and gonads across reproductive castes, linking dopamine pathways and hyperprolactinaemia to eusocial reproductive suppression.