| First Author | Kurz J | Year | 2022 |
| Journal | Development | Volume | 149 |
| Issue | 4 | PubMed ID | 35103284 |
| Mgi Jnum | J:321979 | Mgi Id | MGI:7254929 |
| Doi | 10.1242/dev.199735 | Citation | Kurz J, et al. (2022) Notch signaling is a novel regulator of visceral smooth muscle cell differentiation in the murine ureter. Development 149(4):dev199735 |
| abstractText | The contractile phenotype of smooth muscle cells (SMCs) is transcriptionally controlled by a complex of the DNA-binding protein SRF and the transcriptional co-activator MYOCD. The pathways that activate expression of Myocd and of SMC structural genes in mesenchymal progenitors are diverse, reflecting different intrinsic and extrinsic signaling inputs. Taking the ureter as a model, we analyzed whether Notch signaling, a pathway previously implicated in vascular SMC development, also affects visceral SMC differentiation. We show that mice with a conditional deletion of the unique Notch mediator RBPJ in the undifferentiated ureteric mesenchyme exhibit altered ureter peristalsis with a delayed onset, and decreased contraction frequency and intensity at fetal stages. They also develop hydroureter 2 weeks after birth. Notch signaling is required for precise temporal activation of Myocd expression and, independently, for expression of a group of late SMC structural genes. Based on additional expression analyses, we suggest that a mesenchymal JAG1-NOTCH2/NOTCH3 module regulates visceral SMC differentiation in the ureter in a biphasic and bimodal manner, and that its molecular function differs from that in the vascular system. |
