Pedro P. Rocha

This study develops a new mouse model of encephalocele by over-expressing FGF3, 4, and 15, revealing the absence of posterior commissure and sub-commissural organ as a key developmental defect.

The paper shows that disrupting chromatin domain boundaries with multiple developmental regulators can cause severe gene dysregulation and developmental defects in mice.

The paper investigates how Polycomb Response Elements (PREs) function in the ON transcriptional state, showing that PREs can still loop and interact with enhancers while some PcG proteins remain bound.

This study shows that loss of Ezh2 in the medial ganglionic eminence (MGE) leads to changes in interneuron fate, morphology, and gene expression.

This study shows that MLL3/MLL4 methyltransferase activities are essential for early embryonic development and stem cell differentiation, but their role is lineage-selective and not dependent on enhancer activation.

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 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 demonstrates a two-step mechanism of PRC2-mediated repressive domain formation through nucleation sites and long-range spreading of H3K27me2/3.

The paper introduces 4Tran, a method to study transposon interactions in the genome, revealing their role in chromatin organization and gene regulation.

This paper introduces 4C-ker, a method that improves the reproducibility of identifying genome-wide interactions from 4C-Seq data by accounting for signal biases and varying resolution.