I have a rather varied horizon of interests. I come from a Neuroscience background and worked in learning and memory for years, first in Lymnaea stagnalis and then on Aplisia Californica. For a brief period I switched to schizophrenia endophenotypes in mice before finding a home in zebrafish research looking at energy homeostasis (with a few forays into cancer genetics). 
The focus of my lab is the role of leptin in fish - which in our hands do not get obese. So why not? What does leptin do if it isn't THE adipostat? We have so far slipped into reproductive biology and are looking at leptin signaling in female fish - pioneered by my first grad student!

Re-established that the Lepr LOF really does not become obese in our hands and that leptin signalling is indeed blocked - at least as far as SOCS3 acitvation is concerned. Differences do arise in our hands from even slight variation in holding conditions. Went on to find a reproductive phenotype in zebrafish which is currently the main thrust of the lab - how exactly does leptin modulate reproductive function?

Begleitete Amrutha bei der Aufklärung der Rolle von Leptin bei der Fortpflanzung. Verteidigte seine BSc-Arbeit am 30.01.2023 und ist seitdem zurückgekommen, um die Genotypisierung zu erlernen und sein Projekt voranzutreiben, um es hoffentlich bis zur Veröffentlichung zu bringen.

Recently joined the lab in order to figure out what triggers leptin signalling in our fish!

Worked on Fin Regeneration and the leptin system. Found out that the LepR LOF did not affect fin regeneration as we previously found. Did a lot of tracing back as to what may be the cause for the lost phenotype between Vanderbilt and Germany but sadly to no avail - the phenotype is lost for now.