Doctoral defense in biomedical and health sciences - Fatich Mechmet

On Monday, September 22, 2025, Fatich Mechmet will defend his doctoral thesis at the Faculty of Medicine, University of Iceland.
The thesis is titled: Role of MITF in olfactory bulb neurons: Putative MITF target genes in neurons and the effects of its loss in the aging olfactory bulb.

The opponents are Dr. Alexander Fleischman, Associate Professor at Brown University, Rhode Island, and Sævar Ingþórsson, Associate Professor at the Faculty of Nursing and Midwifery, University of Iceland.

The supervisor was Professor Pétur Henry Petersen. Other members of the doctoral committee were Professor Margrét Helga Ögmundsdóttir, Professor Ragnhildur Þóra Káradóttir, and Associate Professor Sigríður Rut Franzdóttir.

Professor Sædís Sævarsdóttir, Dean of the Faculty of Medicine, will chair the ceremony, which will take place in the Ceremonial Hall of the University of Iceland (Hátíðasalur) and begin at 1:00 p.m.

Abstract

Microphthalmia-associated transcription factor (MITF) is a master regulator in melanocytes and plays and important role in mast cells. Mitf is also expressed in the mitral and tufted (M/T) cells which are projection neurons (PNs), in the olfactory bulb (OB). Lack of MITF leads to neuronal hyperactivity in primary M/T cells but the general function of MITF in neurons is currently unknown.

In this study, putative MITF target genes in M/T cells of mice were identified. They differ from target genes in other cell types including melanocytes and can be grouped into two categories: those likely to be involved in inhibiting neuronal activity and those specific to a subgroup of tufted called middle tufted cells (mTCs). This work also shows that the mTCs are reduced in number in the absence of Mitf, suggesting a role for Mitf in the generation or survival of the mTCs and/or their function. Altered response to odors is also observed in Mitfmi-vag9/mi-vga9 mice, indicating a role of MITF in olfactory adaptation.

Aging affects various brain structures and sensory systems, including the OB, resulting in a decline in olfactory ability. Decline in the OB is associated with early signs of neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. However, the underlying reasons remain unclear. Primary PNs from OBs of young Mitfmi-vga9/mi-vga9 mice show hyperactivity, potentially linked to reduced expression of the potassium channel subunit Kcnd3/Kv4.3, which impacts intrinsic plasticity. In aged Mitfmi-vag9/mi-vag9 mice, reduced olfactory ability was observed without any signs of neuroinflammation or reduction in neuronal number. An increase in the expression of genes coding for potassium channel subunits was found in the OBs of aged Mitfmi-vga9/mi-vga9 mice. This suggests that increased expression of potassium channel subunits in aging Mitfmi-vga9/mi-vga9 mice may compensate for or stabilize neuronal hyperactivity observed in the OB of young Mitfmi-vga9/mi-vga9 mice.

About the doctoral candidate

Fatich Mechmet was born in 1991 in Komotini, in northeastern Greece. He graduated from the natural sciences track of Komotini Secondary School in 2008. Fatich earned a B.Sc. in Molecular Biology and Genetics from the University of Istanbul, Turkey, in 2013 and a master’s degree in Animal Biotechnology from the School of Agriculture and Veterinary Medicine at the University of Bologna, Italy. His master’s thesis was in the field of neuroscience.

In 2017, Fatich worked as a junior scientist at the Algarve Biomedical Research Institute in Portugal, in a research group focused on molecular neuroscience and gene therapy. He began his Ph.D. studies in neuroscience at the University of Iceland in 2018. His research project received funding from the Icelandic Research Fund and the University of Iceland’s Eimskip Fund. Alongside his doctoral studies, Fatich was awarded a teaching assistantship for Ph.D. students and participated in teaching at the University.

Since 2023, Fatich has been working as Chief Biologist at a biotechnology company in Reykjavík.