Activation of Integrin Signaling Can Partially Restore BMP Signaling Defects in Collagen IV Mutant Embryos
(A) Diagram showing how a potential loss of integrin signaling in collagen IV mutant embryos may reduce BMP signaling (left), which would be predicted to be rescued by constitutively active integrin signaling (right).
(B) Expression of TorsoDβPScyt, but not wild-type βPS, can partially restore expression of Race in collagen IV (viking) mutant embryos. Race expression patterns were classified as normal, weak, or lost (n = 3, >70 embryos counted per genotype in each experiment; error bars represent SEM). Asterisks denote significant difference from no transgene control (i.e., 0% rescue); ∗p < 0.05 (t test). See Supplemental Experimental Procedures for details of rescue quantification.
(C) The ush expression pattern is narrower in collagen IV (viking) mutant embryos than in embryos lacking β integrin (βPS−). ush width shown as individual measurements and mean ± SD, n > 45 for each genotype; ∗∗∗∗p < 0.0001 (ordinary one-way ANOVA).
(D) Maternal/zygotic LanB11B1 mutant embryos show a broadened Race expression pattern. Race width shown as individual measurements and mean ± SD, n > 35 for each genotype; ∗∗∗∗p < 0.0001 (Welch’s test). Scale bars represent 50 μm.
(E) Western blot of pMad and transfected Flag-Mad (total Mad), Flag-TkvQD, and Myc-βPS in S2R+ cells which were plated on either plastic or collagen IV and treated with increasing levels of laminin, as indicated.