Department of Molecular and Tumor Pathology, Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuo-Ku, Chiba, 260-8670, Japan.
Department of Pathology, Saitama Medical Center, Saitama Medical University, 1981 Kamoda, Kawagoe, Saitama, 350-8550, Japan.
Sci Rep. 2023 Nov 27;13(1):20913. doi: 10.1038/s41598-023-46866-7.
Notch signaling is an evolutionarily conserved mechanism required for numerous types of cell fate decisions in metazoans. It mediates short-range communication between cells with receptors and ligands, both of which are expressed on the cell surfaces. In response to the ligand-receptor interaction, the ligand and the extracellular domain of the Notch receptor (NECD) in the complex are internalized into ligand-expressing cells by endocytosis, a prerequisite process for the conformational change of the membrane proximal region of Notch to induce critical proteolytic cleavages for its activation. Here we report that overexpression of transmembrane 2 (TM2) domain containing 3 (TM2D3), a mammalian homologue of Drosophila melanogaster Almondex (Amx), activates Notch1. This activation requires the ligand-binding domain in Notch1 and the C-terminal region containing TM2 domain in TM2D3. TM2D3 physically associates with Notch1 at the region distinct from the ligand-binding domain and enhances expression of Notch1 on the cell surface. Furthermore, cell surface expression of Notch1 and Notch2 is reduced in Tm2d3-deficient cells. Finally, amx-deficient Drosophila early embryos exhibit impaired endocytosis of NECD and Delta ligand, for which surface presentation of Notch is required. These results indicate that TM2D3 is an element involved in Notch signaling through the surface presentation.
Notch 信号通路是一种进化上保守的机制,对于后生动物中多种类型的细胞命运决定都至关重要。它介导细胞间的短程通讯,其中受体和配体都表达在细胞表面。在配体-受体相互作用的过程中,复合物中的配体和 Notch 受体(NECD)的细胞外结构域通过内吞作用被内化到表达配体的细胞中,这是 Notch 膜近端区域构象变化的先决条件,进而诱导其激活所需的关键蛋白水解切割。在这里,我们报告跨膜 2 结构域蛋白 3(TM2D3)的过表达会激活 Notch1。这种激活需要 Notch1 的配体结合域和 TM2D3 中的 C 端区域包含的 TM2 结构域。TM2D3 与 Notch1 在不同于配体结合域的区域物理结合,并增强 Notch1 在细胞表面的表达。此外,在 Tm2d3 缺陷细胞中,Notch1 和 Notch2 的细胞表面表达减少。最后,amx 缺陷的果蝇早期胚胎表现出 NECD 和 Delta 配体内化受损,而 Notch 的表面呈现是其内化所必需的。这些结果表明,TM2D3 是 Notch 信号通路通过表面呈现参与的一个组成部分。