Axon myelination is essential for rapid saltatory conduction of nerve impulses in the vertebrate nervous system. A central feature of several of these pathological conditions in the peripheral nervous system (PNS) is the destruction of myelin and the reprogramming of myelinating Schwann cells to a 'progenitor-like' state, a highly unusual feature in mammals.  This rests on the surprising plasticity of Schwann cells that allows them to switch between differentiation states. The work of in the laboratory addresses a set of interlocking issues in Schwann cell biology that deal with Schwann cell myelination, and the response of Schwann cells to pathological conditions. More specifically, we are focused on identifying the key mechanisms that drive Schwann cell reprogramming in different pathological conditions, including nerve injury, genetic disorders, immune cell attack and microbial infections. For these, we have been examining the role of autophagy, and the role of DNA methylation, histone modifications and non-coding RNAs in this process using high-throughput techniques. Another related ongoing project in the lab on is focused on the identification of therapeutical targets for neurofibromatosis type 1 and malignant peripheral nerve sheath tumours (MPNST)