DC 7: Lukas Vaišvilas

Lukas Vaišvilas (Lithuania) has an academic background in pharmaceutical sciences, with a particular emphasis on in vitro disease modelling in the context of neurological disorders. During his master’s programme, he conducted his thesis research at the Masereeuw Lab at the Utrecht Institute for Pharmaceutical Sciences, where he contributed to the development of a blood-brain barrier-on-chip platform to investigate neurological complications associated with chronic kidney disease.

Following his thesis, he joined the Zhang Lab at Harvard Medical School as a research fellow, where he worked on developing a novel organ-on-chip system simulating the innervation of the proximal tubule.

Planned secondments: 3 months at Mimetas for TSC and TREK1 mutant kidney on a chip. 2 months at Fondazione Telethon (TIGEM) for TFEB/S6K interaction in ependymal cells of TSC mutants. 2 months at IMol for establishing TREK1 mutants in Zebrafish

 

Mimetas

3 months
Leiden, the Netherlands

FTELE

3 months
Pozzuoli, Italy

IMOL

2 months
Warsaw, Poland

My research project

Genetic diseases, such as Tuberous Sclerosis Complex (TSC), leading to the up-regulation of mTOR activity predispose to altered cortical development, now classified as mTORopathies, which are associated with epilepsy as well as intellectual disability and autism. However, why aberrant mTOR activity alters neuronal excitability remains unknown. By genetic epistasis experiments in mouse models of the disease, our preliminary data identified one mTOR substrate, S6 kinases 1 (S6K1), as an essential factor for cortical malformations and seizures in a mouse model of TSC. By phospho-proteomics and electrophysiological studies, we observed that S6K1 phosphorylates key determinants of neuronal excitability. We hypothesized that their regulation by S6K1-mediated phosphorylation may contribute to epileptic seizures in Tuberous Sclerosis. The PhD candidate will test this model by original pharmacological, nutritional, biophysical and genetic approaches.