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EMBO | EMBL Symposium: The ageing genome: from mechanisms to disease
June 4, 2023 to June 7, 2023
This conference will take place at EMBL Heidelberg, with the option to attend virtually. Please see EMBL’s COVID-19 safety policy for testing and other requirements if attending the on-site event.
“Time stands still for no one” or for no molecule, for that matter. Of the molecules that undergo changes over time, it is chromosomal alterations that may have some of the most profound and long-lasting cellular and organismal effects. In contrast to any other macromolecule, the genome is irreplaceable and requires constant repair. Despite sophisticated genome maintenance mechanisms, DNA damage accumulates over time and hence with age. The ensuing chromosomal alterations may lead to genome instability, somatic mutations, impaired gene expression and DNA replication, alterations of the epigenetic code and chromatin structure. These molecular processes can impair cell function and alter cell fate thus contributing to disease, tissue and organ dysfunction thus driving the ageing process of the organism.
Therefore, to promote lifelong health it is critical to gain a better understanding of how DNA damage contributes to the ageing process and age-related disease. Similarly, it will be vital to understand how the regulation of DNA repair and genome maintenance changes over the course of ageing. Finally, we need to consider how time-dependent DNA alterations can impinge in gene expression and chromatin structure. Together, a more complete understanding of these interactions will open doors for therapeutic interventions aimed to promote healthy ageing.
This symposium brings together a diverse group of researchers using a breadth of experimental model systems and organisms with a focus on genome maintenance, from DNA repair to chromatin regulation. We hope that by looking at the genome maintenance specifically in the context of ageing, we will gain insights into how chromosomal defects can be avoided, or even repaired during the aging process to ensure optimal cellular function and to promote lifelong health.
- Endogenous and metabolic genotoxins
- Loss of proteostasis
- Telomere dysfunction
- Age related disease
- Model systems for ageing research
- Senescence responses
- DNA repair during the ageing process
MAR 13: Abstract Submission
APR 24: Registration (On-site)
MAY 29: Registration (Virtual)