Macrophage-derived RNAseT2 stimulates muscle stem cell fusion via SLK/N-WASP/actin bundling

Michele Weiss-Gayet, Gaetan Juban, Emmeran Le Moal, Antonio Moretta, Camilla Farnetari, Christelle Gobet, Jules Guillemaud, Marie-Catherine Le Bihan, Oded Shoseyov, Annie Adrait, Katharina Ternka, Odile Boespflug-Tanguy, Matthias Kettwig, Yohann Coute, Remi Mounier, Francesco Acquati, Robert Knight, Benedicte Chazaud
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Abstract

Muscle stem cells (MuSCs) fuse to form myofibers to repair skeletal muscle after injury. Within the regenerative MuSC niche, restorative macrophages stimulate MuSC fusion, although the molecular mechanisms involved are largely unknown. Here, we show that restorative macrophages secrete ribonuclease T2 (RNAseT2) to stimulate MuSC fusion. RNAseT2 entered MuSCs via the mannose receptor and induced the formation of actin bundles in MuSCs, enabling cell/cell fusion. Mechanistically, RNAseT2 bound to Ste20-like kinase (SLK), which itself triggered the phosphorylation-mediated activation of N-WASP, through Paxillin phosphorylation, allowing actin bundling necessary for MuSC fusion. In vivo, overexpressing RNAseT2 in regenerating muscle increased fusion in newly formed myofibers in mouse and zebrafish while macrophages deficient for RNAseT2 gene led to fusion defect and smaller myofibers. This study reveals a new function for the highly conserved RNAseT2 and provides a new molecular mechanism by which restorative macrophages support MuSC fusion during muscle repair.
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巨噬细胞衍生的RNAseT2通过SLK/N-WASP/肌动蛋白束刺激肌肉干细胞融合
肌肉干细胞(MuSCs)融合形成肌纤维,以修复损伤后的骨骼肌。在可再生的MuSC生态位内,恢复性巨噬细胞可刺激MuSC融合,但其中的分子机制尚不清楚。在这里,我们发现恢复性巨噬细胞分泌核糖核酸酶T2(RNAseT2)来刺激MuSC融合。RNAseT2通过甘露糖受体进入MuSCs,并诱导MuSCs中肌动蛋白束的形成,从而实现细胞/细胞融合。从机制上讲,RNAseT2与Ste20样激酶(SLK)结合,SLK本身通过Paxillin磷酸化引发N-WASP磷酸化介导的活化,使肌动蛋白束成为MuSC融合所必需的。在体内,在再生肌肉中过表达 RNAseT2 可增加小鼠和斑马鱼新形成肌纤维的融合,而缺乏 RNAseT2 基因的巨噬细胞会导致融合缺陷和更小的肌纤维。这项研究揭示了高度保守的 RNAseT2 的新功能,并提供了恢复性巨噬细胞在肌肉修复过程中支持造血干细胞融合的新分子机制。
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