6 February 2024

Lundbeck Experiment


Two grants supporting wild research at Department of Biology.

Associate Professor Godefroid Charbon from Section of Functional Genomics received app. DKK 2 mio for the project:
Transforming a bacterium into a neuron powerhouse

Godefroid Charbon

The project aims to identify environmental cues that favor the selection of poorly functioning mitochondria that carries mutations in their DNA. DNA mutations carried by mitochondria are commonly associated with neurologic diseases. Neurons can harbor a mix of wild type and mutated mitochondria. The accumulation of certain mutations determines the severity of neurological disorders. How these mutations are selected despite the presence of several hundred copies of wild type DNA in an individual mitochondrion is not known. We will engineer a bactechondrion, a bacterium-mitochondrion hybrid. This model system will be used to find conditions that favor the selection of mutations.  

Professor Søren Tvorup Christensen from
Section of Cell Biology and Physiology received app. DKK 2 mio for the project:
Deciphering convergence of primary cilia and defects in brain development in Huntington's disease

Søren Tvorup Christensen

Huntington ́s disease (HD) is an inherited disorder that causes the death of nerve cells in the brain, leading to the progressive decline in a person ́s control of movements and loss of higher level processes such as consciousness, thought, memory and emotion. The time from the first symptoms to death is about 10 to 30 years depending on the age of disease onset and severity of mutations in the gene encoding the protein Huntingtin (HTT). However, despite intense research during the last 30 years, there is no cure for HD. Here, we present a novel hypothesis on HD mechanisms and causality, which could redefine the field of HD and deliver novel platforms for developing treatment regiments. Our model depicts that HTT under normal conditions is required for correct formation of the brain via the action of so-called primary cilia, which function as cellular antenna-like organelles in the developing cortex. In this scenario, we predict that mutations in HTT lead to primary cilia defects, whereby the brain is abnormally developed and becomes more vulnerable to degeneration later in life. Such ciliary defects will be deciphered in human stem cell models and cortex organoids, also known as mini brains in a dish. If correct, primary cilia will be a promising target for drug development and early treatment in HD mutation carriers.

Find the news at Lundbeckfonden


Ass. professor Godefroid Charbon

Section of Functional Genomics, Department of Biology

Mail: godefroid.charbon@bio.ku.dk

Tel +45 3532 2098

Professor Søren Tvorup Christensen

Section of Cell Biology and Physiology, Department of Biology

Mail: stchristensen@bio.ku.dk

Tel: +45 5132 2997