Miroslav Radman

Mediterranean Institute for Life Sciences (MedILS)


Election Year: 2018
Primary Section: 26, Genetics
Secondary Section: 21, Biochemistry
Membership Type: Foreign Associate

Biosketch

Miroslav Radman is a geneticist and molecular biologist recognized for some of his ground-breaking work on DNA repair, recombination and mutation and their impact on biological evolution and human health. He is known for: (i) the discovery (with Dr. Evelyn Witkin) of the SOS response to DNA damage, particularly in relation to the genesis of mutations, (ii) the discovery of DNA mismatch repair (together with Drs. Matthew Meselson and Robert Wagner) – the key genetic editing system assuring the fidelity of DNA replication and recombination, that generates genetic barriers between closely related species (speciation) and, recently, (iii) establishing the role of oxidative damage to proteins in cellular resistance to radiation and desiccation, as well as in aging and age-related diseases. M. Radman was born in 1944 in Split (Croatia), grew up on island Hvar, attended high school in Split, graduated biology from University of Zagreb (1966) and received PhD in molecular biology in 1969 from the University of Brussels. After postdoctoral research, first with Raymond Devoret (1969/70) in French CNRS and then with Matthew Meselson at Harvard (1970-73), he became in 1972 associate professor of molecular genetics at the University of Brussels. He moved to Paris in 1983 as research director in French CNRS to found the Laboratory of Mutagenesis at the Institute J. Monod. In 1998 Radman became professor of cell biology at the Medical School of the University of Paris-5. Retired as exceptional class professor emeritus in 2013, he moved to his native Split where he founded in 2004 private not-for-profit Mediterranean Institute for Life Sciences (MedILS) to study the biology of aging and age-related diseases. He was elected (chronologically) to EMBO, Croatian Academy of Sciences and Arts, French Academy of Science, World Academy of Arts and Sciences, European Academy of Science, European Academy of Microbiology, American Academy of Arts and Sciences and US National Academy of Science. He was knighted by the Presidents of Croatia and France and served (2004-2008) as special science advisor to the Prime Minister of Croatia. M. Radman received one dozen of major national and international science prizes and promoted biological science in France and Croatia through over one hundred editorials and interviews in the newspapers and on radio and television broadcasts.

Research Interests

Over four decades of the studies of molecular mechanisms, and enzymes, assuring genetic stability (DNA repair) and variability (mutagenesis and recombination) were crowned by direct visualization of emerging individual mutation and recombination events in single living bacterial cells, in real time. The interest in extreme radiation resistance of the bacterium Deinococcus radiodurans changed the course of Radman's research. His group discovered the mechanism of repair of over one thousand of DNA double-strand breaks per D. radiodurns cell and found that the evolved protection of proteins against oxidative damage accounts for extreme biological robustness. Radman's group showed that biological function can be reduced or destroyed directly by oxidative protein damage (and not only indirectly by mutation). Hence, the view of cell function, aging and survival changed from DNA-centric to protein-centric. Having found that most proteins from aerobic organisms are quasi inoxidable, Miroslav Radman's laboratory studies the causes of protein damage and explores how silent mutations (polymorphisms) sensitize the affected proteins to oxidation and therefore predispose to relevant age-related disease. Furthermore, Radman studies now the mechanism of expression of aging and disease phenotypes and why is long latency of age-related diseases shortened by chronic inflammation. The long term goal of this research is the mitigation of all age-related diseases by prevention and healing by phenotypic reversion. This approach aims to reduce disease initiation (at the genome level) and extend its latency period (at proteome level) to delay the onset of disease, or revert the disease back to health.

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