CTCF point mutation at R567 disrupts mouse heart development via 3D genome rearrangement and transcription dysregulation [4C-seq]
In this study, we performed 4C sequencing to investigate alterations in chromatin interactions mediated by the Lmod2 promoter and its potential enhancer. Overall design: 4C-seq was performed using wild-type and Ctcf homozygous mutation in heart tissues from E18.5 mouse embryos. The region for Lmod2 promoter and its potential enhancer was used as a viewpoint.