Introducing Ioanna Michou DC5
My PhD goals: Establish 2D and 3D cellular models that recapitulate the cystic fibrosis (CF) phenotype via CRISPR-Cas9 genetic engineering and perform high content screening to facilitate drug discovery and validation in CF.
My Background: I obtained a bachelor’s degree in Biological Sciences from the University of Patras, Greece. During my postgraduate studies, I specialized in molecular and cellular biology by attending the master’s program ‘From fundamental molecular biosciences to biotherapies’ (Cancer Biology track) at Sorbonne University, in partnership with Heidelberg University and DKFZ, Heidelberg. Before embarking on my PhD journey, I accumulated valuable work experience and enhanced my critical thinking by conducting various research internships at well-renown European research centres such as CIC, Salamanca, DKFZ, Heidelberg and Institut Gustave Roussy, Villejuif.
My research interests: Biomedical engineering, molecular biotechnology, confocal microscopy, disease modeling, organoids, drug testing
My hobbies: I enjoy practicing ceramics/pottery, going to the gym and spending time in nature with friends.
Master thesis: ‘Unravelling the mechanisms of supracellular polarization during Collective Amoeboid Migration (CAM) in colorectal cancer’
Collective cell migration is known to play an important role in a multitude of physiological processes and its deregulation is associated with cancer. Recently, a new mode of collective cell movement termed Collective Amoeboid Migration (CAM) was discovered by the Jaulin Lab after extensively studying the migration of digestive cancer cell clusters in confined non-adhesive environments. This mode of migration is powered, among others, by actomyosin contractility and specifically by the formation of an actin cage at the rear of the moving cluster. The goal of this research project is to elucidate front-to-rear (F/R) polarity at the supracellular level, and shed light onto additional polarity factors that might be involved in the cluster’s polarity asymmetry establishment during CAM. By performing a small immunofluorescence screening of core factors of the cell polarity machinery in clusters that migrated in non-adhesive microchannels, atypical protein kinase C (aPKC) was found enriched at the rear of the cluster in the form of a supracellular cap. Furthermore, Scribble, a basolateral polarity factor, was found to be anticolocalized with aPKC at the cluster’s peripheral cortex. Exploring how the F/R polarity of these markers emerges during CAM, I found that actomyosin contractility impairment led to a significant decrease in aPKC polarization, whereas inhibition of aPKC mildly decreased actin polarization and cluster speed. These data suggest that aPKC is probably downstream of actin polarization. To conclude, aPKC can be characterized as a robust marker of supracellular polarity leading the way for further real-time study of the mechanisms involved in polarity symmetry breaking and propagation during collective cell migration.