Figure 1.

Loss of Integrin Expression Causes Defects in BMP Signaling Responses in the Early Embryo

(A) Early Drosophila embryo showing patterning of the dorsal ectoderm by a gradient of BMP activity.

(B) RNA in situ hybridizations of wild-type or maternal/zygotic mys^XG43 mutant (βPS⁻) embryos showing expression of the BMP target genes Race, hnt, and ush. For Race and hnt quantification, n = 3, >15 embryos per genotype in each experiment; error bars represent SEM. For ush width, individual measurements are shown with mean ± SD (n = 92 for wild-type and n = 69 for βPS⁻). ^∗∗∗∗p < 0.0001 (unpaired t test).

(C) RNA in situ hybridizations for Race and hnt in mew (mew^M6) and scb (scb^5J38) mutant embryos. Phenotypes were classified as “lost,” “weak,” or “broad” (see Supplemental Experimental Procedures and Figure S2B for details) and were counted on embryo samples collected from heterozygous mutant stocks (n = 3, >60 embryos counted per genotype in each experiment; error bars represent SEM).

(D) pMad immunostaining of wild-type, maternal βPS⁻ zygotic βPS⁺ (mat βPS⁻ zyg βPS⁺) and maternal/zygotic βPS⁻ (βPS⁻) embryos. All scale bars represent 50 μm.

(E–G) Quantification of the pMad gradient in mat βPS⁻, zyg βPS⁺, and βPS⁻ embryos. (E) Mean pMad intensity along the dorsal-ventral axis at 0.5 embryo length. Threshold lines indicate the width of the pMad gradient plotted in (C) and (D). (F and G) Mean width of the pMad gradient at thresholds 0.4 (C) and 0.6 (D) along the anterior-posterior axis for stage 6 embryos. Black dots indicate significant differences (p < 0.05) between maternal βPS⁻ zyg βPS⁺ and βPS⁻.

All embryo images show dorsal views of stage 6 embryos, anterior to the left. See also Figures S1 and S2.