I joined the lab in October of 2015 as an EMBO postdoctoral fellow. I did my PhD project in Barcelona focused on the study of the link between adherens junctions and Wnt signalling in colon cancer cell lines. Following my interest in adherens junctions and cell organisation, I came to the lab to analyse the organization and function of E-Cadherin in pluripotency with a special focus on its interaction with p120-catenin.
There are different kinds of embryonic stem cells: Mouse embryonic stem cells (mESC) that exhibit a naive or ground pluripotency state; and mouse epiblast stem cells (mEpiSCs) and human stem cells (hESCs) that have a primed status of pluripotency. An important difference between them is the organization of E-Cadherin which in EpiSCs is localized to adherens junctions and polarized whereas in mESC cells it is delocalized around the cells. These evidences suggest a role of cell polarity in pluripotency that has been recently emphasized with the discovery that maintenance of naive pluripotency requires an inhibitor of aPKC, a protein that regulates cell polarity in epithelia. Moreover, increases in ÃŸ-catenin in naive ES cells promote pluripotency, whereas increases in EpiSC lead to differentiation. Thus, there might be different complexes between E-Cadherin, and the associated proteins in ES and EpiSCs which regulate the pluripotent state. To test this, I propose to analyze the expression, localization and function of cadherins in the context of adherens junction formation and Wnt signalling.