Research at MedILS is currently grouped under 5 themes:

Genetics of death in yeast

Most, if not all, organisms age and die, but it is not clear whether aging and death are just unavoidable consequences of life or if these processes have some evolutionary advantage and are genetically controlled. This project is motivated by the question why and how the process of dying occurs in eukaryotic cells. To shed more light on this issue, using the advantages of the yeast experimental system, the project focuses on investigation of endogenous causes and deleterious molecular processes leading to cell death by studying all of 1100 genes required for yeast survival and growth.
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Biology of robustness

Life’s robustness depends on the resilience of fertile organisms (the soma) that assure the long-term evolutionary success of the germ-line, i.e., species. In the framework of this project we explore the chemistry of two types of biological clocks: the species-specific somatic clock (robustness of the proteome and life span) and the universal germ-line clock (mutations and evolution). As model organisms, we explore the bacterium D. radiodurans and aquatic animals bdelloid rotifers as well as complex animals like tardigrades, all equally resistant to long-term desiccation and extreme doses of ionizing radiation.
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Molecular basis of intrinsic aging and its prevention

Cellular life is maintained by the activity of a plethora of functions that prevent molecular damage from occurring in the first place and repair damaged DNA, proteins and other damaged cellular constituents. The phenomenon of aging arises from the fact such functions are performed by proteins that are themselves subject to damage by oxidative modifications. In the framework of this project, aging is studied as a process of progressive functional degeneracy of nearly all cellular functions due to diminishing protein activity and decreased precision of protein interactions within the cellular proteome caused by accumulation of oxidative damage.
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Protein carbonylation by cluster enhanced fluorescence in the context of aging

The use of fluorescent markers is a commonly used technique for detecting protein carbonylation. For this purpose organic chromophores such as DNPH have been standardly used. In this project we propose to further enhance the performance of such markers by exploiting cluster enhanced absorption and fluorescence. Such an enhancement effect is required in order to enable in vivo detection of the carbonylation. The advantage of using metal clusters is that they are biocompatible, soluble, robust in terms of optical properties and small enough to go through the cell membranes in contrast to quantum dots. Therefore, small clusters in combination with optical markers such as DNPH are potentially important for sensitive detection and quantification of carbonylation sites
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Mechanisms of neurodegeneration

Accumulation and aggregation of disease-causing proteins is a hallmark of several neurodegenerative disorders such as Parkinson’s, Alzheimer’s and Huntington’s disease. One of the main goals of research in neurodegenerative disorders has been to improve clearance of accumulated proteins. This project is focusing on using molecular and genomic approaches to identify common mechanisms that lead to neurodegeneration. Strategies are developed in order to selectively activate cellular degradation machinery to improve clearance of mutant proteins and identify novel therapeutic targets for the treatment of neurodegenerative disorders
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