Rafael D. Acemel

The paper investigates the evolution of CTCF's role in chromatin organization across species, finding that vertebrate CTCF enables loop extrusion but requires additional factors for full genome architecture.

This study presents a multi-omic atlas of the siphonophore Physalia utriculus, revealing the regulatory mechanisms of colonial division of labour and the molecular basis of venom activity.

The paper identifies supporting-like cells as an alternative steroidogenic lineage in mammals, conserved across amniotes, and shows their role in embryonic development and evolution.

The paper compares single-cell transcriptomic data from turtles, mice, and chickens to show divergence in gonadal cell types and genetic programs across sex determination systems.

The paper studies regulatory genome evolution in echinoderms, revealing deep conservation of cis-regulatory elements and chromatin organization, suggesting an ancestral regulatory pattern in animal genomes.

This study shows pluripotency factors like OCT4 and NANOG initially repress and later enable activation of lineage specifiers, including the HoxB cluster, during early embryonic development.

The paper investigates how clustered-CTCF boundaries function in vivo, showing that individual CTCF sites can override other factors and that insulation strength modulates gene expression and phenotypes.

The paper creates a central repository for zebrafish developmental genomics data, identifies new cis-regulatory elements, and compares regulatory elements between zebrafish and mouse.

The paper identifies regulatory elements and chromatin structures in the RCA gene cluster, revealing long-range interactions and a TAD boundary within CR1 that influence gene expression and autoimmune disease susceptibility.

This study shows that CTCF knockout in zebrafish disrupts chromatin structure and gene regulation during development, affecting thousands of genes and developmental programs.

The paper identifies cis-regulatory elements in the zebrafish and human pancreas, revealing disease-related enhancers that affect gene expression and contribute to pancreatic disorders.