Lars Wittler

Prime-editing lineage trees for 16 mouse embryos (E7.5 to E10.0, >1.4 million cells) quantify fate restriction timing, progenitor numbers and lineage relationships, and are reproducible across replicate embryos.

The paper shows that activation of an LTR retrotransposon in the embryo leads to viral-like particle production, causing limb malformations through apoptotic cell death.

The paper describes a method to achieve targeted sex ratio distortion in mice using a selfish supergene component, resulting in a high prevalence of non-transgenic offspring of the desired sex.

The study identifies two enhancer elements that maintain En1 expression during later limb development and shows that misexpression timing leads to distinct phenotypes.

The paper shows that microRNA activity is essential for early mouse embryos to transition into diapause, with miRNAs regulating gene expression and linking mTOR activity to miRNA biogenesis.

The paper identifies thousands of notochord enhancers, including TNE2, using ATAC-seq and in vitro models, showing their role in T expression and tail development in mouse embryos.

The paper uses single-cell RNA sequencing to systematically phenotype mouse genetic models, identifying molecular and cellular changes across multiple mutants and wildtypes.

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 investigates how clustered-CTCF boundaries function in vivo, showing that individual CTCF sites can override other factors and that insulation strength modulates gene expression and phenotypes.

The paper investigates how Polycomb-mediated genome architecture facilitates long-range H3K27 methylation spreading in ESCs and iPSCs, revealing RNA-dependent DNA looping and developmental gene roles in chromatin organization.

The paper investigates how genomic rearrangements at the Lbx1/Fgf8 locus cause SHFM3 by altering chromatin structure and gene expression in mice.

The paper shows that divergent gene expression within TADs is resolved through TAD restructuring and DNA methylation, not enhancer-promoter compatibility or position.

This paper introduces a CRISPR-Cas9-engineered mouse model for GPI-anchor deficiency that mirrors human phenotypes, including cognitive impairments and epilepsy, and identifies synaptic transmission deficits.

This study investigates the emergence and patterning dynamics of mouse definitive endoderm using in vivo and in vitro models, revealing self-sorting and Sox17 expression patterns.

The paper describes a method to generate trunk-like structures from mouse embryonic stem cells that mimic embryonic development features.

The paper shows that preformed chromatin topology supports robust Shh transcription during limb development, with CTCF and ZRS alleles influencing enhancer-promoter communication.

The paper investigates TAD function in mice by editing TAD organization, finding that TADs provide robustness but are not essential for gene regulation, and that disease phenotypes arise from re-direction of regulatory contacts.