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Esco2 restrains pathological endothelial-to-mesenchymal transition through hidden isoform regulation in a Roberts syndrome model

ABSTRACT: ESCO2 encodes a cohesin acetyltransferase required for embryonic development, but how ESCO2 deficiency disrupts endothelial cell state and vascular development remains incompletely understood. This study used conditional Esco2 deletion in embryonic yolk sac endothelium to investigate gene-expression, transcript-isoform, and chromatin-occupancy changes associated with endothelial dysfunction. Short-read single-cell RNA sequencing of E9.5 control and Esco2-deficient yolk sacs was used to define endothelial and endothelial-to-mesenchymal transition (EndMT)-associated cell states. Single-cell long-read isoform sequencing (ScISOr-seq) was used to resolve transcript isoform usage and identify isoform switching not apparent from gene-level expression. In parallel, Esco2 CUT&Tag was performed on FACS-isolated GFP+ Lyve1-lineage cells from E9.5 yolk sacs to define genomic regions associated with Esco2 occupancy. Together, these datasets provide complementary gene-level, isoform-level, and chromatin-occupancy profiles for investigating Esco2-dependent regulation of endothelial state during early vascular development.

ORGANISM(S): Mus musculus

PROVIDER: GSE344313 | GEO | 2026/09/14

REPOSITORIES: GEO

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