| First Author | Tanaka Y | Year | 2023 |
| Journal | Dev Cell | Volume | 58 |
| Issue | 16 | Pages | 1447-1461.e6 |
| PubMed ID | 37413993 | Mgi Jnum | J:339246 |
| Mgi Id | MGI:7520706 | Doi | 10.1016/j.devcel.2023.06.002 |
| Citation | Tanaka Y, et al. (2023) Nodal flow transfers polycystin to determine mouse left-right asymmetry. Dev Cell 58(16):1447-1461.e6 |
| abstractText | Left-dominant [Ca(2+)](i) elevation on the left margin of the ventral node furnishes the initial laterality of mouse embryos. It depends on extracellular leftward fluid flow (nodal flow), fibroblast growth factor receptor (FGFR)/sonic hedgehog (Shh) signaling, and the PKD1L1 polycystin subunit, of which interrelationship is still elusive. Here, we show that leftward nodal flow directs PKD1L1-containing fibrous strands and facilitates Nodal-mediated [Ca(2+)](i) elevation on the left margin. We generate KikGR-PKD1L1 knockin mice in order to monitor protein dynamics with a photoconvertible fluorescence protein tag. By imaging those embryos, we have identified fragile meshwork being gradually transferred leftward involving pleiomorphic extracellular events. A portion of the meshwork finally bridges over the left nodal crown cells in an FGFR/Shh-dependent manner. As PKD1L1 N-term is predominantly associated with Nodal on the left margin and that PKD1L1/PKD2 overexpression significantly augments cellular Nodal sensitivity, we propose that leftward transfer of polycystin-containing fibrous strands determines left-right asymmetry in developing embryos. |
