I began my PhD project at the Charité Institute shortly after moving to Berlin in the end of April of this year. Unfortunately, I had what I would qualify as a bit of a rough start. I had moved to another country before a few years ago already and thus thought I had an understanding of what to expect, but I underestimated how much of a challenge not being fluent in the language was going to be, especially with regard to finding a place to live. Additionally, I had to learn to perform long and complicated experiments unlike anything I had done previously. This, combined with a host of administrative issues, meant that the first few months of my PhD project were more difficult than anticipated.
And although luckily these issues did end up slowly but surely resolving themselves, the ALLODD workshop in Barcelona was still fortuitously timed. The change of pace, the interesting lectures and especially the opportunity to finally meeting my fellow ESRs from the program in person for the first time (as well as a number of the PIs) as I was unfortunately unable to attend the first workshop meeting in Vienna physically. The setup also facilitated networking, which I can otherwise find a bit daunting.
I was especially reminded of how interesting the field of GPCRs can be, both in academia and in the industry, and this comforted me in my decision to do a PhD centering on the study of the GPCR MC3R was indeed the right choice for me.
Furthermore, MC3R in particular seems to be on the rise in terms of the interest accorded to it by the scientific community. Indeed, it has been considered in the past to have a redundant role to its relative MC4R due to both having loss of function mutations connected to obesity. However, as it turns out the phenotype of these mutations for MC3R, unlike MC4R, includes an increase of the fat mass compared to lean mass as well as the mice models having trouble putting weight back after a period of restricted feeding. Moreover, several studies have also shown that MC3R variants in both mice and human patients result in the late onset of puberty and abnormal menstrual cycles, as well as a lowered expression of several genes in the circadian rhythm. Despite these observations of how MC3R mutants affect organisms’ phenotype, information regarding the intracellular trafficking of MC3R is unfortunately lacking due to commercially available MC3R antibodies being non-specific in their binding.
This makes the study of MC3R, specifically of its structure and its ligand binding affinity, particularly fascinating as it could very well elucidate some of the mystery that still surround this protein’s function, and I hope I will be able to take steps towards doing so in the coming months. I look forward to continuing improving my skills and pursuing my career both at the Charité Institute and within the ALLODD program.