Apratim Mitra

The paper analyzes young KRAB-zinc finger gene clusters in mice, showing ERVs drive genetic heterogeneity through recombination and duplication mechanisms.

The paper uses integrated bulk, single-cell, and spatial RNA-seq to uncover the timeline of osteogenic transcriptional programming in embryonic palate development, identifying novel genes and spatial expression patterns involved in palatal fusion.

The paper shows that high affinity enhancer-promoter interactions can bypass CTCF/cohesin insulation and maintain gene expression in some tissues but not others.

The paper shows GATA6 and NANOG bind shared regulatory elements to drive divergent cell fates in mouse blastocysts by modulating chromatin accessibility and transcriptional activation.

The paper characterizes the epigenomic landscape of embryonic mouse forebrain neural progenitors using snATAC-Seq and integrates multi-omics data to reveal region-specific regulatory mechanisms.

This study shows that reducing Wapl dosage partially corrects transcriptome and growth defects in Nipbl-/+ embryonic mouse brains, suggesting cohesin dynamics regulate gene expression.

This study uses single-cell RNA sequencing to reveal transcriptional heterogeneity in ventricular zone cells of the embryonic mouse forebrain, showing spatial and temporal gene expression differences.

This study identifies Grin1 as a key regulator of subtype-specific gene expression in MGE-derived interneurons, linking NMDAR signaling to neurodevelopmental disorders like schizophrenia.

The paper shows that maternal loss of imprinting at the H19/IGF2 locus causes cardiac pathologies in mice, with Igf2 driving transient hypertrophy and H19 causing progressive fibrosis and reduced ventricular function.

This study identifies OTUD5 as essential for chromatin remodeling during development, showing its role in preventing degradation of chromatin regulators and maintaining proper gene expression networks.

The paper shows that deleting large KRAB-ZFP gene clusters in mice leads to retrotransposon activation, indicating most KRAB-ZFPs are non-essential for transposon suppression.