I want to thank all the co-authors (on bluesky @davidbrueckner.bsky.social, and @saren-t.bsky.social) and the @heisenbergcplab.bsky.social members. This work was possible thanks to the great work of the ISTA facilities, in particular the Fish Facility and the Imaging & Optics Facility.

Here our model of how LME animal migration ends. I am happy to see this work out! As for cell migration in vivo, the path of this journey hasn’t always been straightforward. It is the closing of a chapter, and I look forward to what the future will bring.

Without BMP signalling, LME doesn’t converge to the dorsal side, the last part of the LME migration. Is BMP also needed to onset the tumbling motion? Yes! When we depleted BMP from the animal ectoderm, the ectoderm became cohesive, and LME migration no longer stopped.

We tested that by changing the animal's or lateral ectoderm's tissue cohesiveness before transplantation. We increased in the animal ectoderm and decreased in the lateral one, which was sufficient to inverse the effect on LME migration. What does modulate the cohesiveness of the ectoderm?

We noticed that the animal ectoderm thins faster than the lateral one, suggesting that the tissue properties differ. Specifically, we found that the animal ectoderm is loosened and less cohesive. Does the difference in cohesiveness regulate LME animal migration?

The ectoderm could have a different permissiveness to LME migration at the animal pole than the lateral side. We tested it with transplantation experiments and found that the animal ectoderm impairs LME migration while the lateral one promotes it. What does determine the different permissiveness?

I hypothesized that the substrate could tell the LME when and where to stop the animal migration. We first found that the LME migrates on the ectoderm, which the epiboly causes to move passively in the opposite direction. Does the ectoderm cause the LME to start tumbling?

This is the case of the lateral mesendoderm (LME) in the early zebrafish gastrula. At this stage, LME migrates on the lateral side of the embryo from the margin towards the animal pole. However, it never reaches it and, instead, it starts tumbling. My question was: why does LME animal migration end?

When we think of cell migration, we often think of extracellular matrix (ECM), whether the focal adhesion-dependent mesenchymal migration or the confinement-dependent amoeboid migration. But what if cells move without ECM and don’t even need confinement?

That is a great reason for a first post! With a few days of delay, I am proud to share that my postdoc work at the @heisenbergcplab.bsky.social has finally been published on @cp-cellreports.bsky.social doi.org/10.1016/j.ce... Now a small (or maybe not) thread about the work!

Without BMP signalling, LME doesn’t converge to the dorsal side, the last part of the LME migration. Is BMP also needed to the onset the tumbling motion? Yes! When we depleted BMP from the animal ectoderm, the ectoderm became cohesive, and LME migration no longer stopped.

We tested that by changing the animal's or lateral ectoderm's tissue cohesiveness before transplantation. We increased in the animal ectoderm and decreased in the lateral one, which was sufficient to inverse the effect on LME migration. What does modulate the cohesiveness of the ectoderm?

We noticed that the animal ectoderm thins faster than the lateral one, suggesting that the tissue properties differ. Specifically, we found that the animal ectoderm is loosened and less cohesive. Does the difference in cohesiveness regulate LME animal migration?

The ectoderm could have a different permissiveness to LME migration at the animal pole than the lateral side. We tested it with transplantation experiments and found that the animal ectoderm impairs LME migration while the lateral one promotes it. What does determine the different permissiveness?

I hypothesized that the substrate could tell the LME when and where to stop the animal migration. We first found that the LME migrates on the ectoderm, which the epiboly causes to move passively in the opposite direction. Does the ectoderm cause the LME to start tumbling?

This is the case of the lateral mesendoderm (LME) in the early zebrafish gastrula. At this stage, LME migrates on the lateral side of the embryo from the margin towards the animal pole. However, it never reaches it and, instead, it starts tumbling. My question was: why does LME animal migration end?

When we think of cell migration, we often think of extracellular matrix (ECM), whether the focal adhesion-dependent mesenchymal migration or the confinement-dependent amoeboid migration. But what if cells move without ECM and don’t even need confinement?