Benoit Bruneau

@benoitbruneau.bsky.social

Cardiac developmental biologist. Oakland and San Francisco. Hi friends! 🇨🇦

Visually, it looks like they're just =disapparating=. Beam me up, Mr. Bug. They have a sort of hidden spring under their bellies, called a 'furca' or 'furcula'. Like having a secret catapult hidden down your trousers. I love the lowering of the antennae just before launch. 💨

Thrilled to see this published today! Truly special because we made the initial discovery >15 yrs ago! We found two copies of a human gene called BC200 embedded in a human poxvirus. BC200 blurs the line between gene & transposon—both functional & mutagenic! www.science.org/doi/10.1126/... 🧵1/n

Escape of the BC200 gene to a human poxvirus reveals its persistent transposition in primates

Transposable elements mobilize within and occasionally between genomes, including from host to virus. We identified two insertions of the human BC200 noncoding RNA gene in the poxvirus molluscum conta...

science.org

1\ We know a bit about how 3D chromatin interactions are formed, but what do we know about how they are disrupted? We asked this question in our latest preprint: doi.org/10.64898/202..., focusing on the massive loss of promoter interactions during neuronal differentiation.

Developmentally programmed loss of long-range Polycomb interactions is regulated by cohesin

Distal regulatory elements (DREs), such as enhancers, can regulate genes across megabase-long distances, presumably via coming into close spatial proximity. The establishment of new transcriptional programmes during cell type transitions is associated with widespread rewiring of the spatial organisation of the genome, including gain and loss of chromatin interactions. Extensive effort has been invested into understanding how chromatin interactions are formed during development, yet the mechanisms underlying their developmental loss remain largely unclear. By leveraging chromatin accessibility-assisted footprinting, acute protein degradation and chromatin conformation capture, we show that loss of promoter interactions cannot be explained by reduced binding of sequence-specific transcription factors (TFs). Instead, we identify a subset of interactions that depend on cohesin for programmed developmental disruption. These sites are characterized by high Polycomb enrichment and TF occupancy and engage in strong long-range interactions that undergo extensive differentiation-dependent rewiring. Preventing interaction loss by acute cohesin degradation results in the preferential downregulation of associated genes. Together, these results suggest that cohesin indirectly regulates developmental loss of Polycomb interactions by enabling the acquisition of other potentially regulatory contacts in a process that may shape transcriptional programs during cell type transitions. ### Competing Interest Statement The authors have declared no competing interest. European Research Council Helmholtz Society, VH-NG-1604

doi.org

sad to learn that Terri Grodzicker has passed. She was the founding editor of @genesdev.bsky.social and instantly made it a phenomenally important journal. Over 35 years as editor she brought the most important science to an eager audience. It is rare to find someone with such a breadth of knowledge