skip to primary navigationskip to content

Benedicte Sanson Projects

Supervisor: Bénédicte Sanson


Project 1: Role of the adhesion molecule Sidekick in adherens junction remodeling during developmental morphogenesis

 We have identified the adhesion molecule Sidekick, which was known for its role in synaptogenesis in the visual system, as the first component of tricellular adherens junctions (tAJs) in developing epithelia (1, 2).  Epithelia change shape extensively during embryo development and this requires the remodeling of the contacts between cells, which include adherens and occluding junctions. Whereas there is knowledge about how bicellular contacts are remodeled, less is known about tricellular contacts, the “cell corners”. Cell behaviours important to shape tissues such as polarised cell intercalation, cell division and cell extrusion require the remodelling of cell-cell contacts, posing a conformational problem at tricellular junctions that has started to be addressed. Also there is evidence that tricellular vertices are important for tension sensing and force transmission during epithelial remodelling. Until recently, resident proteins at tricellular contacts were known only for occluding junctions, both in vertebrates (angulins and tricellulins) and in invertebrates (Gliotactin, Anakonda, M6) (3). The identification of Sidekick gives an opportunity to study the role of tricellular adherens junctions. Recent studies, including from our group, show that Sidekick facilitates polarized cell intercalation in four different tissues in Drosophila (2). The goal of this PhD project is to follow-up on these findings and investigate the mechanisms by which Sidekick contributes to junctional remodeling, using the early Drosophila embryo as a model. Approaches will include super-resolution (live and fixed) microscopy to follow Sdk localization during remodeling, photoactivation techniques to ask how adherens junction components and the actomyosin cytoskeleton are redistributed around tAJs, molecular and cellular approaches to elucidate a pathway that localizes Sdk at cell corners.

Relevant references:

1.  Lye, C. M., Naylor, H. W. and Sanson, B. (2014). Subcellular localisations of the CPTI collection of YFP-tagged proteins in Drosophila embryos. Development 141, 4006-4017.

2.  T. Finegan*, N. Hervieux*, A. NestorBergmann, A. Fletcher, G. Blanchard, 

B. Sanson (2019). The tricellular vertex-specific adhesion molecule Sidekick facilitates polarised cell intercalation during Drosophila axis extension. BioRxiv 704932; (accepted at PloS Biology)

3.  Higashi T, Miller AL. Tricellular junctions: how to build junctions at the TRICkiest points of epithelial cells. Molecular Biology of the Cell. 2017;28(15):2023-34. doi: 10.1091/mbc.E16-10-0697.


Project 2: Regulation of cell number during axis extension.

Tissue elongation is a very common morphogenetic movement, crucial for both axis elongation at gastrulation but also the morphogenesis of organs and tissues later in development (kidney, cochlea, jaw etc.) (1). Tissue elongation (called also convergence and extension) is caused by cells intercalating in a polarised manner (2). These cell behaviours require the planar polarisation of cellular components, such as the actomyosin cytoskeleton. One mystery about these movements is how cells can rearrange without disturbing the gene expression patterns already laid out in a given tissue? We have found that in Drosophila embryos, the planar polarisation of actomyosin has in fact a dual role: in addition to triggering polarised cell intercalation through the contraction of specific cell-cell contacts, long-range actomyosin cables form that stop rearranging cells from intermingling (3). We also showed that actomyosin polarisation depends upon cell-cell interactions along the antero-posterior axis, presumably reading differences in receptors at the cell surface controlled by the segmentation cascade (pair-rule genes and upstream regulators). We have evidence that the more different the cells are, the more actomyosin is polarised and the more rapidly cells intercalate (3). Therefore this quantitative system has the potential to regulate cell numbers in the tissue. We propose to test this novel hypothesis by manipulating cell numbers in various ways in early embryos. We plan to use genetic means to make parasegments with too many or too few cells and investigate how the embryos “repair” parasegment size by modulating the rate of polarized intercalation during axis extension. Our established methods will be used to quantify i) cell numbers ii) actomyosin planar polarisation and iii) rates of cell intercalation in manipulated embryos (3).


 1.  Tada M, Heisenberg CP. Convergent extension: using collective cell migration and cell intercalation to shape embryos. Development. 2012;139(21):3897-904. doi: 10.1242/dev.073007.

 2.  Huebner RJ, Wallingford JB. Coming to Consensus: A Unifying Model Emerges for Convergent Extension. Dev Cell. 2018 Aug 20;46(4):389-396. doi: 10.1016/j.devcel.2018.08.003.

3.  Tetley RJ, Blanchard GB, Fletcher AG, Adams RJ, Sanson B. Unipolar distributions of junctional Myosin II identify cell stripe boundaries that drive cell intercalation throughout Drosophila axis extension. Elife. 2016;5:e12094. doi: 10.7554/eLife.12094.


RSS Feed Latest news

Developmental clock and mechanism of de novo polarization of the mouse embryo

Jan 07, 2021

Study by the Zernicka-Goetz lab highlights the role of zygotic genome activation in regulating the timing of cell polarization

View all news