L’équipe Gazave a publié un nouvel article dans Genome Biology and Evolution :
Evolution of apoptotic signalling pathways within lophotrochozoans
Résumé :
Apoptosis is the main form of regulated cell death in metazoans. Apoptotic pathways are well characterised in nematode, fly and mammals, leading to a vision of the conservation of apoptotic pathways in metazoans. However, we recently showed that intrinsic apoptosis is in fact divergent among metazoans. In addition, extrinsic apoptosis is poorly studied in non-mammalian animals, making its evolution unclear. Consequently, our understanding of apoptotic signalling pathways evolution is a black-box which must be illuminated by extending research to new biological systems. Lophotrochozoans are a major clade of metazoans which, despite their considerable biological diversity and key phylogenetic position as sister group of ecdysozoans (i.e. fly, nematode), are poorly explored, especially regarding apoptosis mechanisms. Traditionally each apoptotic signalling pathway was considered to rely on a specific initiator Caspase, associated with an activator. To shed light on apoptosis evolution in animals, we explored the evolutionary history of initiator Caspases, Caspase activators and the BCL-2 family (which control mitochondrial apoptotic pathway) in lophotrochozoans using phylogenetic analysis and protein interaction predictions. We discovered a diversification of initiator Caspases in molluscs, annelids and brachiopods, and the loss of key extrinsic apoptosis components in platyhelminths, along with the emergence of a clade specific Caspase with an ankyrin pro-domain. Taken together, our data show a specific history of apoptotic actors’ evolution in lophotrochozoans, further demonstrating the appearance of distinct apoptotic signalling pathways during metazoan evolution.
Horkan HR, Popgeorgiev N, Vervoort M, Gazave E, Krasovec G. Evolution of apoptotic signalling pathways within lophotrochozoans. Genome Biol Evol. 2024 Sep 25:evae204. doi: 10.1093/gbe/evae204. Epub ahead of print. PMID: 39318156.