{"id":2019,"date":"2018-11-21T09:27:13","date_gmt":"2018-11-21T09:27:13","guid":{"rendered":"http:\/\/blogs.kent.ac.uk\/biosciences\/?p=2019"},"modified":"2018-11-21T09:27:13","modified_gmt":"2018-11-21T09:27:13","slug":"research-seminar-transcriptomic-signature-of-longevity-in-c-elegans","status":"publish","type":"post","link":"https:\/\/blogs.kent.ac.uk\/biosciences\/2018\/11\/21\/research-seminar-transcriptomic-signature-of-longevity-in-c-elegans\/","title":{"rendered":"Research Seminar: Transcriptomic signature of longevity\u00a0in\u00a0C. elegans"},"content":{"rendered":"

Dr<\/b>. <\/b>Collin Ewald<\/b>, ETH Zurich, Institute for Translational Medicine, Department of Health Sciences and Technology<\/strong><\/p>\n

Tuesday 27th November, <\/b>12.00 noon, Ingram Lecture Theatre<\/b><\/span><\/p>\n

Aging is the progressive decline of physiological integrity\u00a0and function of an organism over time ultimately leading to the onset of\u00a0age-dependent\u00a0diseases. Longevity interventions, such as caloric restriction and reduced\u00a0insulin\/IGF-1 signaling, slow down the\u00a0aging process. The nematode\u00a0Caenorhabditis <\/i>elegans<\/i>\u00a0is\u00a0a key model\u00a0system to study the role of aging and longevity. In the current literature,\u00a0there is an abundance of studies describing gene expression changes\u00a0associated\u00a0with longevity. However, we currently lack an overall conceptual understanding\u00a0of how the individual longevity interventions are related. Do longevity\u00a0interventions\u00a0share downstream targets or act via distinct mechanisms and are there genes, which\u00a0consistently accompany longevity?<\/p>\n

To\u00a0answer these questions, we re-analyzed published longevity expression profiles (190\u00a0arrays, 130 sequencing runs) to directly\u00a0compare longevity regulation across\u00a0studies. We extracted and combined the gene expression changes caused by all\u00a0known\u00a0longevity interventions in\u00a0C.\u00a0<\/i>elegans<\/i>\u00a0to identify the underlying gene expression signatures that might\u00a0promote healthy aging. By re-analyzing the published datasets with a common pipeline,\u00a0we are able to correct for variations arising from different laboratory\u00a0conditions or used strains to extract the changes that are more\u00a0longevity-specific. The majority of genes we found to be\u00a0differentially\u00a0expressed across longevity interventions in\u00a0C.\u00a0<\/i>elegans<\/i>\u00a0are downregulated during physiological aging. Intriguingly,\u00a0longevity interventions display a large overlap in their targeted pathways\u00a0indicating a shared mode of action. To expand the view\u00a0offered by annotated\u00a0pathways, we performed a GO term enrichment and identified the extracellular\u00a0matrix genes as a key target\u00a0enriched in both aging and longevity. Our\u00a0comparative approach revealed a more robust network of gene expression changes\u00a0shared\u00a0by longevity intervention. These findings can be directly used to generate\u00a0hypothesis to reveal novel mechanisms that promote\u00a0healthy aging.<\/p>\n