CLASPs maintain BM integrity during EMT through their MT-binding ability. (A) Schematic diagram of human CLASP1α and human CLASP2γ, and deletion mutants of human CLASP2 used in this study. (B and C) Effect of eGFP-CLASP2-ΔMΔC overexpression. White arrowheads in B indicate the streak midline. White arrows in B indicate normal BM breakdown in streak midline cells. White arrows in C indicate that CLASP2-ΔMΔC–overexpressing cells in lateral epiblast region have premature laminin breakdown. (D) Percentage of expressing cells showing laminin breakdown. Phenotypes are classified into three categories: no breakdown, mild breakdown, and complete breakdown. ΔMΔC (77.6%, n = 134 cells from six embryos) and ΔC (78.1%, n = 105 cells from four embryos) showed severe phenotypes. ΔM mutant showed a mild phenotype (35.6%, n = 90 cells from four embryos) in comparison with control GFP (14.3%, n = 105 cells from five embryos). (E) Knockdown of CLASP1 protein by CLASP1-specific MOs caused laminin breakdown. White arrows indicate ectopic BM breakdown in lateral epiblast cells. (F) 5mis-control MO does not affect laminin expression. Yellow arrows indicate normal BM levels in 5mis-CLASP1 control MO–receiving cells. (G) Percentage of MO-containing cells showing laminin breakdown with different MOs. CLASP1 MO, 88.8% (n = 107 cells from five embryos); CLASP2 MO, 51.8% (n = 112 cells from three embryos); CLASP1 + CLASP2 MOs, 75.6% (n = 86 from three embryos); 5mis CLASP1 control MO, 14.8% (n = 115 from three embryos). Bars, 20 µm.