Spatial focalization of pheromone/MAPK signaling triggers commitment to cell-cell fusion.

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2016

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info:eu-repo/semantics/altIdentifier/doi/10.1101/gad.286922.116

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info:eu-repo/semantics/altIdentifier/pmid/27798845

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info:eu-repo/semantics/altIdentifier/pissn/0890-9369

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info:eu-repo/semantics/altIdentifier/urn/urn:nbn:ch:serval-BIB_0017F15B0B987

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O. Dudin et al., « Spatial focalization of pheromone/MAPK signaling triggers commitment to cell-cell fusion. », Serveur académique Lausannois, ID : 10.1101/gad.286922.116


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Cell fusion is universal in eukaryotes for fertilization and development, but what signals this process is unknown. Here, we show in Schizosaccharomyces pombe that fusion does not require a dedicated signal but is triggered by spatial focalization of the same pheromone-GPCR (G-protein-coupled receptor)-MAPK signaling cascade that drives earlier mating events. Autocrine cells expressing the receptor for their own pheromone trigger fusion attempts independently of cell-cell contact by concentrating pheromone release at the fusion focus, a dynamic actin aster underlying the secretion of cell wall hydrolases. Pheromone receptor and MAPK cascade are similarly enriched at the fusion focus, concomitant with fusion commitment in wild-type mating pairs. This focalization promotes cell fusion by immobilizing the fusion focus, thus driving local cell wall dissolution. We propose that fusion commitment is imposed by a local increase in MAPK concentration at the fusion focus, driven by a positive feedback between fusion focus formation and focalization of pheromone release and perception.

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