Ruth L. and David S. Gottesman Institute for Stem Cell and Regenerative Medicine Research, Bronx, NY, USA.
Department of Cell Biology, Albert Einstein College of Medicine, Bronx, NY, USA.
Nat Commun. 2021 May 4;12(1):2522. doi: 10.1038/s41467-021-22749-1.
Haematopoietic stem cells (HSCs) tightly regulate their quiescence, proliferation, and differentiation to generate blood cells during the entire lifetime. The mechanisms by which these critical activities are balanced are still unclear. Here, we report that Macrophage-Erythroblast Attacher (MAEA, also known as EMP), a receptor thus far only identified in erythroblastic island, is a membrane-associated E3 ubiquitin ligase subunit essential for HSC maintenance and lymphoid potential. Maea is highly expressed in HSCs and its deletion in mice severely impairs HSC quiescence and leads to a lethal myeloproliferative syndrome. Mechanistically, we have found that the surface expression of several haematopoietic cytokine receptors (e.g. MPL, FLT3) is stabilised in the absence of Maea, thereby prolonging their intracellular signalling. This is associated with impaired autophagy flux in HSCs but not in mature haematopoietic cells. Administration of receptor kinase inhibitor or autophagy-inducing compounds rescues the functional defects of Maea-deficient HSCs. Our results suggest that MAEA provides E3 ubiquitin ligase activity, guarding HSC function by restricting cytokine receptor signalling via autophagy.
造血干细胞(HSCs)在整个生命周期中通过严格调控其静息、增殖和分化来生成血细胞。这些关键活动如何平衡的机制仍不清楚。在这里,我们报告称,巨噬细胞-成红细胞附着器(MAEA,也称为 EMP),一种迄今为止仅在成红细胞岛上发现的受体,是一种膜相关的 E3 泛素连接酶亚基,对 HSC 的维持和淋巴样潜能至关重要。 Maea 在 HSCs 中高度表达,其在小鼠中的缺失严重损害了 HSC 的静息状态,并导致致命的骨髓增生性综合征。从机制上讲,我们发现几种造血细胞因子受体(例如 MPL、FLT3)的表面表达在没有 Maea 的情况下得到稳定,从而延长了它们的细胞内信号转导。这与 HSCs 中的自噬通量受损有关,但与成熟造血细胞无关。受体激酶抑制剂或自噬诱导化合物的给药可挽救 Maea 缺陷的 HSCs 的功能缺陷。我们的研究结果表明,MAEA 提供 E3 泛素连接酶活性,通过自噬限制细胞因子受体信号来保护 HSC 功能。