Department of Pathology & Laboratory Medicine, Robert Wood Johnson Medical School, Rutgers University, Piscataway, New Jersey, USA.
Department of Biochemistry and Microbiology, Institute for Quantitative Biomedicine, Rutgers University, Piscataway, New Jersey, USA.
J Biol Chem. 2024 Jul;300(7):107429. doi: 10.1016/j.jbc.2024.107429. Epub 2024 Jun 1.
Polymerizing laminins are multi-domain basement membrane (BM) glycoproteins that self-assemble into cell-anchored planar lattices to establish the initial BM scaffold. Nidogens, collagen-IV and proteoglycans then bind to the scaffold at different domain loci to create a mature BM. The LN domains of adjacent laminins bind to each other to form a polymer node, while the LG domains attach to cytoskeletal-anchoring integrins and dystroglycan, as well as to sulfatides and heparan sulfates. The polymer node, the repeating unit of the polymer scaffold, is organized into a near-symmetrical triskelion. The structure, recently solved by cryo-electron microscopy in combination with AlphaFold2 modeling and biochemical studies, reveals how the LN surface residues interact with each other and how mutations cause failures of self-assembly in an emerging group of diseases, the LN-lamininopathies, that include LAMA2-related dystrophy and Pierson syndrome.
聚合层粘连蛋白是具有多个结构域的基底膜 (BM) 糖蛋白,可自行组装成细胞锚定的平面晶格,从而建立初始 BM 支架。随后,巢蛋白、胶原-IV 和蛋白聚糖会在不同的结构域附着在支架上,以形成成熟的 BM。相邻层粘连蛋白的 LN 结构域相互结合形成聚合物节点,而 LG 结构域则附着在细胞骨架锚定整合素和 dystroglycan 上,以及附着在硫酸脑苷脂和肝素硫酸上。聚合物节点是聚合物支架的重复单元,组织成近对称的三腿蛋白。该结构最近通过冷冻电子显微镜结合 AlphaFold2 建模和生化研究得到解决,揭示了 LN 表面残基如何相互作用,以及突变如何导致一组新兴疾病——LN-层粘连蛋白病,包括与 LAMA2 相关的营养不良和 Pierson 综合征中的自组装失败。