Are they bicoid and caudal? How did the 17th Century Tibet get this????AMAZING!

😅Please add me to both "morphogenesis" and "collective cell migration". Thank you, Maik!

Hi Maik, Thanks very much for creating the starter packs. Could you please add me?

Last but not least, huge thanks to all co-authors, Dr. Yasuhiro Inoue, Masaya Hayashi, and Dr. John Wallingford @jbwallingford.bsky.social . Special thanks to the editor, Dr. Deborah Taylor, for her guidance, and the reviewers for their invaluable feedback.

Figure 6: When scaling up to tissues, CE spreading and propagation are essential. In Arvcf-deficient tissue, disrupted t-junction rotation is correlated to localized and discontinuous convergence, showcasing an impaired multiscale mechanical synergy at play.

Figure 5: Using a dynamic vertex model, we found that a single t-junction rotation can trigger cascading cell intercalations, spreading CE across the tissues. A biomechanical domino effect!

Figure 4: Our static toy models reveal how perpendicular t-junctions block force coupling and propagation, demonstrating how microscale defects escalate to large-scale abnormalities.

Figure 3: Our previous work on Arvcf revealed its role in maintaining cell cortex tension. Interestingly, Arvcf depletion delays t-junction rotation, leading to many more perpendicular t-junctions. This subtle change in cell packing is indeed akin to a “traffic jam”.

Figure 2: T-junction rotation is driven by a “four-way tug-of-war” between tensions on connected v-junctions. We employed a non-invasive image-based analysis to confirm this tension-based mechanism. Please stay tuned for more details on this method.