| First Author | Xin Q | Year | 2023 |
| Journal | Dev Cell | Volume | 58 |
| Issue | 18 | Pages | 1716-1732.e8 |
| PubMed ID | 37714160 | Mgi Jnum | J:341141 |
| Mgi Id | MGI:7532499 | Doi | 10.1016/j.devcel.2023.08.025 |
| Citation | Xin Q, et al. (2023) Chromatin remodeling of prostaglandin signaling in smooth muscle enables mouse embryo passage through the female reproductive tract. Dev Cell 58(18):1716-1732.e8 |
| abstractText | Early mammalian development occurs during embryo transit of the female reproductive tract. Transport is orchestrated by secreted oviduct fluid, unidirectional beating of epithelial cilia, and smooth muscle contractions. Using gene-edited mice, we document that conditional disruption of a component of the SWI/SNF chromatin remodeling complex in smooth muscle cells prevents transport through the oviduct without perturbing embryogenesis. Analysis with RNA sequencing (RNA-seq), transposase-accessible chromatin with sequencing (ATAC-seq), chromatin immunocleavage sequencing (ChIC-seq), and pharmacologic rescue experiments implicated prostaglandin signaling pathways. In comparison with controls, gene-edited mice had compromised chromatin accessibility at enhancer/promoters of Ptgs2, Pla2g16, Pla2r1, and Ptger3 (EP3) as well as decreased enhancer-promoter interactive looping critical for Ptgs2 (aka Cox-2) expression in a SWI/SNF complex-dependent manner. Treatment of wild-type mice with prostaglandin inhibitors phenocopied the genetically induced defect. |
