Why? What is the specific question or hypothesis being tested for this figure? H

Question

Why? What is the specific question or hypothesis being tested for this figure?

How? Methods: Describe how the experiment was performed.

What? Results. Summarize the experimental results, highlighting the relevant controls and main conclusions that can be made only from the data in this figure.

So what? Conclusions. Summarize the conclusions from this figure (and only this figure!)

C Donor NCC cdh6SplMO Hos Fig. 4. Cdh6 function in EMT is NCC autonomous and Cdh6-GFP rescues morpholino knockdown. (A) Cell nject showing NCCs that were in the neuroepithelium at imaging onset. Time-lapse imaging began at 14 hpf. Yellow dashed lines mark basal neuroepithelial surfaces and white dashed lines mark apical midlines. (C) A wild-type donor NCC (red/green) undergoes EMT normally when transplanted into a Cdh6 knockdown embryo. (D) NCCs expressing Cdh6-GFP undergo EMT as a cluster in Cdh6 knockdown embryo. Time-h:min:s. Scale bars: 10 um. 00:00:00 00:06:00 00:15:30 00:15:30 D cdh6SpIMO NCC-Cdh6-GFP 00:00:00 :48:17 1:15:03

Explanation / Answer

Answer to the first part of the question:-

The epithelial-to-mesenchymal transition (EMT) could be a complicated modification in cell constitution that's vital for cell migration, morphogenesis and carcinoma metastasis. Loss of epithelial cell adhesion and tight regulation of cadherin adhesion proteins are crucial for EMT. Cells undergoing EMT typically show cadherin change, wherever they downregulate one cadherin and induce expression of another. Neural crest cells (NCCs), that endure EMT throughout development, lose N-cadherin and upregulate Cadherin 6 (Cdh6) before EMT. Cdh6 has been recommended to suppress EMT via cell adhesion, however conjointly to push EMT by mediating pro-EMT signals.

Here the experiment is being conducted to determine novel roles for Cdh6 in generating cell motility during EMT. Tests being done by live imaging of NCC behavior in vivo to point out that Cdh6 promotes detachment of top NCC tails, a crucial early step of EMT. moreover, this study shows that Cdh6 affects spatiotemporal dynamics of F-actin and active rho GTPase which Cdh6 is needed for accumulation of F-actin in top NCC tails throughout detachment. Together, this information recommend that Cdh6 is a very important determinant of wherever subcellular protein forces are generated throughout EMT. These results additionally determine mechanisms by that an upregulated cadherin will generate cell motility throughout EMT.

Now come to the particular figure that is given here :-

They generated mosaic embryos via blastula stage cell transplantations, to test whether or not Cdh6 operate in EMT is NCC-autonomous. All cells were labeled with Texas Red-dextran and NCCs additionally expressed GFP in donor embryos. Cdh6 morpholinos were injected to host embryo. Donor cells were transplanted at 3 hpf and host embryos were imaged at 14 hpf. Donor NCCs were known as having each green and red visible radiation. Then they examined solely donor NCCs in areas wherever the epithelium contained no alternative donor-derived wild-type cells (n=12 NCCs in four embryos). Of these, 10 NCCs (83.3%) underwent EMT. (Fig-C) shows one example of a personal donor NCC undergoing the total method of EMT. This knowledge show that individual NCCs with traditional Cdh6 levels will endure EMT once encircled by Cdh6-knockdown cells, indicating that the functions of Cdh6 in detachment and EMT are NCC-autonomous.

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