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What mechanisms ensure healthy aging? Researchers from IUF and HHU in Düsseldorf investigate this in the roundworm, an established organism for aging research. A study which was recently published in EMBO Reports provides new insights into the mechanisms of longevity promoted by reduced mitochondrial activity.
Median life expectancy of our society is still increasing which leads us to the question: how can we extend healthy aging? This is being investigated on a molecular level in the model organism Caenorhabditis elegans*, a transparent round worm with a size of about 1 mm. It is widely used in research on aging processes due to conserved genes and age-associated features in comparison to humans. Up to now, researchers know that interventions that promote healthy aging are typically associated with increased robustness and stress resistance, which is the ability to better prevent harmful influences. Paradoxically, reducing the activity of core biological processes such as mitochondrial (cellular powerhouses) or insulin metabolism promotes the expression of adaptive responses, which in turn increase animal longevity and resistance to stress.
In a study that was recently published in EMBO Reports, Dr. Natascia Ventura’s research group from IUF and HHU in Düsseldorf, Germany, investigated for the first time the relation between the extended C. elegans lifespan elicited by reducing mitochondrial functionality and resistance to genotoxic (gene damage) stress e.g. by irradiation and chemical substances. They found that reducing mitochondrial activity during development confers germline (cells, whose genetic material can be passed on to offsprings) resistance to DNA damage-induced cell cycle arrest and apoptosis (cell death). Interestingly, they showed that although this mechanism requires somatic cells (all other, non-germline cells which are most body cells), it is uncoupled from those required for somatic robustness. Specifically, the C. elegans homologs of the BRCA1 and BARD1 tumor suppressor genes, brc-1 and brd-1, were identified as mediators of the anti-apoptotic effect but dispensable for lifespan extension upon mitochondrial stress. The study was conducted in cooperation with colleagues from Cologne (Germany), Norway and the USA.
“Mitochondria are key organelles required for proper cell and body homeostasis. Long-termed maintenance of mitochondrial function and quality is of vital importance for human health”, states the director of the Central Institute of Clinical Chemistry and Laboratory Medicine of the Heinrich Heine University Düsseldorf, Prof. Fritz Boege. “We try to better understand the molecular mechanisms involved in mitochondrial stress extension of lifespan in order to develop intervention strategies which may allow us to extend healthy aging in the future. One additional aspect investigated in our lab are mitochondrial-associated diseases of genetic or environmental origin, which span from developmental to age-associated pathologies”, explains Dr. Natascia Ventura, who leads a joint liaison group of the IUF – Leibniz Research Institute for Environmental Medicine and the Central Institute of Clinical Chemistry and Laboratory Medicine of the Heinrich Heine University Düsseldorf. “We all strive for a long and healthy life. It will be very exciting to see which insights we can gain in the future and how this will allow us to ultimately promote healthy aging”, adds Prof. Jean Krutmann, director of IUF.
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* About the model organism Caenorhabditis elegans
The roundworm C. elegans is widely used in aging research for several reasons: It is a multicellular organism with a short life cycle and mean lifespan of 15-20 days. Its genome is completely sequenced and more than 60 percent of its genes have the same structure and function of human genes. The worm has a small size of about 1 mm, it is transparent, and it has very well characterized phenotypes (appearance) and behaviors. Remarkably, several age-associated features are conserved between C. elegans and humans: progressive degeneration of different tissues, decline in physiological functions and resistance to stress, and increased probability of death with age. These evolutionarily conserved animal features can be analyzed under the microscope to study the effects of genetic or environmental interventions on the aging process, with important implication for human health.
About the IUF
The IUF – Leibniz Research Institute for Environmental Medicine investigates the molecular mechanisms through which particles, radiation and environmental chemicals harm human health. The main working areas are environmentally induced aging of the cardiopulmonary system and the skin as well as disturbances of the nervous and immune system. Through development of novel model systems the IUF contributes to the improvement of risk assessment and the identification of novel strategies for the prevention / therapy of environmentally induced health damage.
More information: http://www.iuf-duesseldorf.com.
The IUF is part of the Leibniz Association: http://www.leibniz-gemeinschaft.de/en/home.
Contact
Christiane Klasen, Personal Assistant to the institute’s Director
IUF – Leibniz Research Institute for Environmental Medicine
Auf’m Hennekamp 50
40225 Düsseldorf
Germany
Email: Christiane.Klasen@IUF-Duesseldorf.de
Phone: +49 (0)211 3389 216
Torgovnick A, Schiavi A, Shaik A, Kassahun H, Maglioni S, Rea SL, Johnson TE, Reinhardt HC, Honnen S, Schumacher B, Nilsen H, Ventura N: BRCA1 and BARD1 mediate apoptotic resistance but not longevity upon mitochondrial stress in Caenorhabditis elegans. EMBO Rep 2018. doi: 10.15252/embr.201845856. Link: https://www.doi.org/10.15252/embr.201845856
C. elegans’ mitochondria in muscles (red) and intestine (green) are visualized through the expressio ...
A. Schiavi, AG Ventura/IUF
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C. elegans’ mitochondria in muscles (red) and intestine (green) are visualized through the expressio ...
A. Schiavi, AG Ventura/IUF
None
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