This project, started with totally different aims, taught me that in every story there is something more, if you have the curiosity and the patience to look for it.
Intercellular communication regulated by TGFß in the #zebrafish cardiac outflow tract.⬇️ biorxiv.org/content/10.110…
Impossible without the help, the discussions and the input of my amazing colleagues! #stainierlab
Thanks especially to @BensimonBrito and all the other coauthors!
@BensimonBrito I rarely saw such a specific effect of the mutation as in alk5 mutants' outflow tract. And the zebrafish beating heart is always a pleasure to image! 😍
@BensimonBrito And if you re-overexpress alk5 only in the endothelium...it's almost back to normal
• • •
Missing some Tweet in this thread? You can try to
force a refresh
I'm thrilled to share our story about the cellular crosstalk in the developing heart, regulated by TGF-β from the endothelial cells. Below more details and some beautiful #zebrafish hearts ⬇️. Coincidentally, it was out @elife exactly on #WorldHeartDay! ❤️elifesciences.org/articles/57603
When we mutated tgfbr1/alk5 in zebrafish, we found a very specific dilation of the cardiac outflow tract (OFT), resembling mammal aortic aneurysms...while all the other vessels and the heart looked unaffected. Occasionally, we even found ruptures and holes in the OFT!
In contrast with the literature on aneurysms and on TGF-β (focus on smooth muscle cells), we observed that the earliest defect in the increased proliferation of endothelial cells, when we did not even observe any morphological defect yet. Is it here where Alk5 plays a role?