Francois Lallemend

I am an associate professor at the Department of Neuroscience at Karolinska Institute. I received my PhD at the GIGA Neuroscience, in Liege (Belgium), followed by postdoctoral research at the Medical Biochemistry and Biophysics Department at the Karolinska Institute, working on neural crest and cell type diversification. I established my research group in 2011, and have been recruited at the Neuroscience Department in 2013, where I head the lab of neuronal specification and connectivity. The main focus of our research is to investigate how neurons are integrated into functional circuits during development.

Francois Lallemend, Lau grant recipient 2016. Photo by Saida HadjabAn important aspect of this process is the existence of a massive cell death and axonal degeneration program that is activated in the developing vertebrate nervous system and which represents an essential process in the formation of functional neural circuits. The mechanism driving the death of neurons during target innervation is proposed to depend on a competition between neurons for limiting amount of target-derived neurotrophic factors. Axon degeneration and neuronal cell death are also widely observed in a number of neurodegenerative diseases. At the opposite, failures in the processes controlling programmed cell death contribute to tumorigenesis. In this context, many cancers share signaling molecules with developing neurons to control their survival or death. In all those biological processes, the activity of neurotrophic factors (e.g. neurotrophins) and/or of their receptors (e.g. Trk receptors) play crucial role in providing a survival advantage or inducing cell death. This paradoxical role for Trk signaling lies in the fact that binding of neurotrophins to their Trk receptor generates survival signals while in contrast the unbound receptor can trigger apoptosis. Yet, the exact molecular context which participates in promoting survival or death of the Trk-expressing cell is still poorly understood. Also, whether competition for survival is inter-cellular, based on limited availability of neurotrophins at the target, or intracellular, based on inherent cell diversity and differential expression of pro- and anti-apoptotic signaling, remains unknown.

Through the Ming Wai Lau Center collaborative research environment, the lab will focus on elucidating whether competition between neurons is a key determinant of their survival, testing the hypothesis that the integrated action of different pro- and anti-apoptotic factors defines the intrinsic survival capacity of neurons during development. Translational aspect of our research aims to identify key molecular players of neuronal cell death and modulate them in neural tumors to provide new efficient treatment.

Selected publications:

Hadjab S, Franck M, Wang Y, Sterzenbach U, Ernfors P and Lallemend F*. A local source of FGF initiates development of the unmyelinated linage of sensory neurons. J. Neurosci. 2013 Nov;33(45):17656-66

Furlan A, Abdo H, Lubke M, Adameyko I, Enomoto H, Lallemend F and Ernfors P. The transcription factor Hmx1 and growth factor signaling control the fate of sympathetic neurons. EMBO J. 2013 May 29; 32(11):1613-25

Lallemend F*, Sterzenbach U1/Hadjab S1, Aquino JB, Castelo-Branco G, Sinha I, Villaescusa C, Levanon D, Wang Y, Franck M, Linnarsson S, Kharchenko O, Adameyko I, Groner Y, Turner E and Ernfors P*. Positional differences of intrinsic axon growth rates between sensory neurons encoded by Runx3. EMBO J. 2012 Sep 12;31(18):3718-29

CentreRegenerative MedicineStem Cell Biology