Figure 10.

Model of laminin interactions. (a) Laminin-1 and its fragments. (b) β1-Integrin initiates laminin-α1 expression in endoderm, enabling heterotrimer formation and secretion. The laminin becomes anchored to and concentrated on the endodermal (not depicted) and (shown) outer ICM cell surfaces largely via LG4–5, accompanied by recruitment of β1-integrins and α/β-dystroglycan (DG) that interact with LG1–3 and LG4, respectively. Laminin polymerizes through its short arms creating a multivalent network. The ICM, requiring this network, but not requiring integrin or dystroglycan, becomes polarized and converted to epiblast. α6β1-Integrin, interacting with polymerizing laminin through LG1–3, down-regulates dystroglycan (DG), and dystroglycan down-regulates basement membrane components. Type IV collagen forms a second network and nidogen and perlecan are incorporated into a more stable ECM. Mesodermal differentiation is delayed in the laminin-treated integrin-null EBs.