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Results: 3

1.
Fig 1.

Fig 1. From: An allelic series of mutations in Smad2 and Smad4 identified in a genotype-based screen of N-ethyl-N- nitrosourea-mutagenized mouse embryonic stem cells.

Severe embryonic defects associated with Smad2m1Mag mutation. (A and B) Gross morphology of wild-type (A) and Smad2m1Mag/Smad2Robm1 (B) concepti at E11.5. Smad2m1Mag/Smad2Robm1 concepti consist of an empty yolk sac devoid of an embryo proper. (C) Wild-type embryo at E9.5. (DF) Three classes of Smad2m1Mag/Smad2m1Mag embryos at E9.5. (D) The empty yolk sac closely resembles the phenotype observed in Smad2m1Mag/Smad2Robm1 (B). (E) A mass of tissue at the distal tip (arrow) is observed in another class of Smad2m1Mag/Smad2m1Mag embryo. This mass of tissue is contractile, indicating the presence of some cardiac muscle differentiation. (F) The most advanced class of Smad2m1Mag/Smad2m1Mag embryo exhibits many embryonic structures. Note the expanded pericardial cavity (bracket) and truncated anterior neurectoderm (arrowhead).

Jay L. Vivian, et al. Proc Natl Acad Sci U S A. 2002 November 26;99(24):15542-15547.
2.
Fig 2.

Fig 2. From: An allelic series of mutations in Smad2 and Smad4 identified in a genotype-based screen of N-ethyl-N- nitrosourea-mutagenized mouse embryonic stem cells.

Defects in the formation of the dorsal aorta, foregut, and notochord in Smad2m1Mag/Smad2m1Mag embryos. (AD) Hematoxylin and eosin staining of transverse histological sections of wild-type (A and C) and Smad2m1Mag/Smad2m1Mag (B and D) embryos at E9.5 about the level of the heart at ×10 (A and B) and ×20 (C and D) objective magnification. Smad2m1Mag/Smad2m1Mag embryos display a small foregut (FG) compared with wild type and lack a morphologically obvious notochord (No). (E and F) Ventral view of the dorsal aortae (DA) at the region of the opening of the foregut of intact wild-type (E) and Smad2m1Mag/Smad2m1Mag (F) embryos at E8.5 visualized with an anti-PECAM antibody. Significant endothelial differentiation is observed in mutant embryos but the aorta fails to condense fully. (G and H) Transverse sections of PECAM-stained embryos at the level of the foregut entrance of wild-type (G) and Smad2m1Mag/Smad2m1Mag (H) embryos at E8.5. The cells of the dorsal aortae display strong PECAM expression about the aortic lumen in wild-type embryos. Although PECAM-positive endothelial cells are present in mutant embryos (H, arrowhead), cells fail to form an aortic lumen in this region of the embryo.

Jay L. Vivian, et al. Proc Natl Acad Sci U S A. 2002 November 26;99(24):15542-15547.
3.
Fig 3.

Fig 3. From: An allelic series of mutations in Smad2 and Smad4 identified in a genotype-based screen of N-ethyl-N- nitrosourea-mutagenized mouse embryonic stem cells.

Defects associated with the Smad4m4Mag allele. Hematoxylin and eosin-stained sagittal sections of E7.5 embryos are shown. (A) Wild-type gastrulating embryo showing newly formed mesoderm (arrow) and other well patterned structures. (B) Homozygous Smad4tm1Cxd embryo. (C) Smad4m4Mag/Smad4tm1Cxd embryo. (D) Homozygous Smad4m4Mag embryo. (BD) Compared with the wild-type E7.5 embryo (A), these mutant embryos are much smaller, with no sign of the initiation of gastrulation or the formation of mesoderm. Also note the disproportionally large cavity between the visceral and parietal endoderm (asterisks). (E) Steady-state level of SMAD4 protein in unmutagenized wild-type ES cells (lane 1) and three mutagenized sibling subclones (lane 2, wild-type for Smad4; lanes 3 and 4, heterozygous for Smad4m4Mag). The same blot was stripped and reprobed with an anti-ACTIN antibody to show equal loading of total cellular proteins.

Jay L. Vivian, et al. Proc Natl Acad Sci U S A. 2002 November 26;99(24):15542-15547.

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