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Fosseprez, O.

Publications and source records attributed to Fosseprez, O..

2 recordsLinked to original sources

Nuclear exosome targeting complexes modulate cohesin binding and enhancer-promoter interactions in 3D

Three-dimensional long-range contacts between enhancers and promoters are thought to be largely determined by loop extrusion driven by the cohesin complex and insulator factors. However, recent evidence also suggests a role for noncoding RNAs (ncRNAs), such as enhancer-associated RNAs (eRNAs) and promoter upstream transcripts (PROMPTs), in shaping enhancer-promoter connectivity. While nuclear RNA exosome, together with targeting complexes, PAXT and NEXT, control the decay of ncRNAs, it has not yet been determined whether these complexes regulate 3D contacts. Chromatin recruitment maps of ZCCHC8 (NEXT), ZFC3H1 (PAXT) and MTR4 helicase revealed that these factors that associate with sites of enhancer-promoter interactions. Depletion of NEXT, PAXT or MTR4 induced the accumulation of ncRNAs, notably enhancer-associated RNAs (eRNAs) and promoter upstream transcripts (PROMPTs). Strikingly, this further increased cohesin levels at sites accumulating ncRNAs. Chromatin conformation capture analysis revealed that MTR4 modulates the 3D long-range contacts between enhancers with their distant TSS targets. Upon loss of MTR4, contacts at anchor points increase while intraloop contacts decrease, suggesting that MTR4 facilitates loop extrusion. These data highlight a key interplay between cohesin-mediated enhancer-promoter interactions and the regulation of ncRNAs by nuclear RNA exosome that is consistent with a role for RNA in genome folding.

molecular biology↗

Crosstalk between chromatin and the transcription factor Shavenbaby defines transcriptional output along the Drosophila intestinal stem cell lineage.

The transcription factor Shavenbaby (Svb), the only member of the OvoL family in Drosophila, controls intestinal stem cell differentiation. Post-translational modification of Svb produces two protein isoforms, Svb-ACT and Svb-REP, which promote intestinal stem cell renewal or differentiation, respectively. Using engineered cell lines, we express either isoform to define their mode of action, and develop an unbiased method to identify Svb target genes in intestinal cells. Within a given cell type, Svb-ACT and Svb-REP antagonistically regulate the expression of a set of target genes, binding specific enhancers whose accessibility is constrained by. During intestinal differentiation, the set of target genes progressively changes, together with chromatin accessibility. Moreover, Svb-REP binding stabilizes three-dimensional enhancer-promoter loops, while influencing the local chromatin landscape to repress target genes. We propose that SvbACT-to-REP switch promotes enterocyte differentiation of intestinal stem cells through direct gene regulation and chromatin remodeling.

genomics↗