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Characterization of the in vivo function of actin-associated proteins using transgenic mice


Research objectives and content
Understanding the mechanisms and the regulation of cell motility is a fundamental task for cell biology with far reaching potential for medical applications. Immundeficiencies caused by unresponsive granulocytes, woundhealing and metastasis are conditions in which control of cell motility could be beneficial. This project aims to elucidate the mechanisms by which cells regulate the activity of the actin cytoskeleton and motility. For interpreting and applying the results to medical conditions it is essential to work with a mammalian system as close as possible to men. To date, advances in mouse genetics have made mouse a superior model system for studying basic biological and medical relevant questions. We will use mouse mutants for certain actin binding proteins (gelsolin, capG, profilin) and cells from these mutants to study the effects on the actin cytoskeleton and motility. This will enable us to ask more specific questions in terms of the physiological responses of the mutant mice. We will also investigate the potential adaptation mechanisms which allow the mutant mice to survive despite the genetic defect. Training content (objective, benefit and expected impact)
The main objective is to understand how the complex interactions of actin with its associated proteins lead to the plethora of actin dependent functions observed in mammalian cells. Having a strong background in the biochemical and cell biolgical analysis of the actin cytoskeleton as well as computer programming I will benefit from the possibility to combine these skills. Within this project I can expand my knowledge in cell biology, microscopy and image analysis. EMBL with its excellent scientific environment will be a perfect place to learn these new techniques. Actin dynamic in live cells and motility are fascinating aspects of cell biology which I would like to study in the lively and multidisciplinary environment of EMBL-Monterotondo.
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EU contribution
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