Spatial focalization of pheromone/MAPK signaling triggers commitment to cell-cell fusion.
Spatial focalization of pheromone/MAPK signaling triggers commitment to cell-cell fusion.
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DOI:
10.1101/gad.286922.116
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发表时间:
2016-10-01
影响因子:
10.5
通讯作者:
Martin SG
中科院分区:
文献类型:
--
作者:
Dudin O;Merlini L;Martin SG
Here, Dudin et al. show that cell fusion does not require a dedicated signal but is triggered by spatial focalization of the same pheromone–GPCR–MAPK signaling cascade that drives earlier mating events in Schizosaccharomyces pombe. 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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