Kathryn E. Yost

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.

This study shows that inflammation-induced changes in 3D genome conformation regulate immune signal integration and transcriptional memory in macrophages.

This study uses spatial transcriptomics and lineage tracing to show how tumor subclones drive microenvironmental changes that promote metastasis in a mouse model.

A >50,000-element viral smORF library screened by growth, MHC-I, ER stress, Perturb-seq and mass spectrometry yields >2,000 active microproteins and shows EBV BNLF2b inhibits PKA by mimicry.

PEtracer maps cell state and lineage dynamics in vivo with high spatial resolution using prime editing and multimodal imaging.

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 identifies Hnrnpa2b1 as a key RBP regulating myogenic differentiation through post-transcriptional control in skeletal muscle regeneration.

This paper introduces ENTER-seq, a method using engineered lentiviral particles to systematically discover receptor-ligand interactions and map TCR specificity in single cells.

TCR-BERT uses self-supervised transfer learning on unlabeled T-cell receptor sequences to learn representations that improve antigen-binding prediction, specificity clustering, and computational TCR sequence design.

The paper uses integrated spatial multi-omics to study fibroblast fate during tissue repair and defines mechanisms controlling cell fate in wound healing.

BABEL translates between scRNA-seq and scATAC-seq at single-cell resolution, enabling synthesis of paired multi-omic data when only one modality is available.

This study examines B cell clonal expansion and convergent antibody responses in SARS-CoV-2 patients, identifying shared features with SARS-CoV.

This study shows Spen binds to endogenous retroviral RNAs and recruits chromatin silencing machinery, linking RNA-mediated retrovirus silencing to X chromosome inactivation.

The paper uses scATAC-seq to analyze chromatin accessibility in immune cell development and tumor microenvironments, identifying regulatory elements and trajectories associated with cell differentiation and therapy response.