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Actomyosin boundaries that form during the development and act as mechanical barriers that sort cells during tissue elongation

last modified Jul 08, 2016 12:39 PM
Richard Adams, Guy Blanchard, Benedicte Sanson and Robert Tetley featured on eElife journal

During animal development a single cell, the egg, divides repeatedly to form a ball of cells. This ball then elongates to form the main body axis in a process called gastrulation. From studies of different animal models, including the fruit fly Drosophila, we know that cells intercalate between each other in a coordinated manner. In Drosophila, this is controlled by the genetic program that divides the embryo into repeated units (segmentation). The segmentation program tells the cell to add actomyosin cytoskeleton to their sides, causing them to contract and be pushed past each other.

This mechanism for oriented cell intercalation is well understood at the scale of a few cells. However, we do not know how hundreds of cells can intercalate in a short time without mixing inappropriately or deforming the tissue. We believe that there is way for cells to regulate the intercalation at tissue-scale. To confirm this we monitored the actomyosin enrichment patterns at the scale of the tissue in live embryos.

We found that there there are actomyosin boundaries that form during the development and act as mechanical barriers that sort cells during tissue elongation. We filmed developing embryos in which we highlighted the actomyosin cytoskeleton and the cell membranes with fluorescent markers. Using our own computational tools, we quantified how much actomyosin was enriched in the  cell sides during tissue elongation. As the tissue elongated, we could see how the actomyosin cytoskeleton changed polarity. By averaging the data between six videos, we analyzed up to 2000 cells for a given time point. We found reproducible patterns on which we are basing a model on how the cells intercalate at the tissue scale. Cells along the main body axis acquire a specific identity depending on their position, and cell to cell interactions lets them compare their identities to each other and modify the actomyosin enrichment accordingly. Where identities are different, cells enrich the sides in actomyosin: at the tissue-scale, this leads to the formation of the boundaries between columns of cells of the same identity.

The next step in our research is to check that the patterns we have detected are altered in mutants where the differential identities along the main body axis are disrupted. Some of these mutants are known, others still need to be identified. We predict that in these mutant, the specific boundaries that we have found in our data will be missing.

Benedicte Sanson

Read the full study here.

16 May 2016

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