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. 2020 Sep 8;11:4477. doi: 10.1038/s41467-020-18185-2

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 8 — PGC clusters disperse by utilizing Tre1^−/− to interpret a presumed migratory cue presented at the exterior of the cluster to orient and stabilize individual migratory polarity radially from the cluster. Sustained polarization of myosin II contracts posterior cortices into foci as PGCs separate. Across the cluster, the opposing directions of PGC migration facilitate a collective response by aligning diametric migratory forces, akin to breaking a rope (cell adhesions) by pulling both ends apart. E-cadherin remains present on the cell membrane throughout. In the absence of Tre1^−/−, PGC motility is randomized, resulting in a significant decrease in migration persistence. Clusters remain intact as PGCs are unable to orient their migration in a given direction for a sufficient time period to detach.