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. 2002 Feb;22(3):901–915. doi: 10.1128/MCB.22.3.901-915.2002

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Copyright © 2002, American Society for Microbiology

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FIG. 3. — Paxillin-null embryos display defects in multiple mesodermally derived structures. Timed matings were performed with paxillin^+/− mice and embryos isolated at E7.5 or E8.5. Genotypes of embryos were determined by PCR either with yolk sac DNA or from scraping of sections (data not shown). (A and B) At E7.5 in paxillin^−/− embryos, the amnion (Amn) is collapsed on the embryo and the allantois (All) is misshapen and moving anteriorly rather than dorsally towards the chorion. (C and D) At E8.5, paxillin mutants are significantly smaller overall. No obvious heart structure is present (Ht), and mutants have an abnormal headfold (Hf) and allantois (All). (E to H) Histological sections of wild-type and paxillin-null embryos. The headfold region is smaller than normal, but expected cell populations are present adjacent to the neural groove (NG), including neural epithelium (NE) and cephalic mesenchyme (CM). In contrast, the mutant embryo lacks a cardiogenic plate (CP) and the endodermal lining of the foregut (FG) remains open. The allantois (All) also appears to be abnormal. (G) A more caudal section of a wild-type embryo, in which the notochord (NC) and rostral extension of dorsal aorta (DA) are visible. Adjacent to the primitive streak (PS), mesodermal cells (M) are visible. (H) More caudal section of a paxillin-null embryo, in which the discrepancy in overall headfold size, compared to that of the wild type, is more pronounced. Cephalic mesenchymal (CM) cells appear condensed. Mutant embryos also lack an organized notochord, and the dorsal aorta is absent. Paxillin-null embryos also lack organized somites (in more caudal sections; not shown). In contrast, the primitive streak (PS) and adjacent mesodermal (M) cells appear normal.

FIG. 3. — Paxillin-null embryos display defects in multiple mesodermally derived structures. Timed matings were performed with paxillin^+/− mice and embryos isolated at E7.5 or E8.5. Genotypes of embryos were determined by PCR either with yolk sac DNA or from scraping of sections (data not shown). (A and B) At E7.5 in paxillin^−/− embryos, the amnion (Amn) is collapsed on the embryo and the allantois (All) is misshapen and moving anteriorly rather than dorsally towards the chorion. (C and D) At E8.5, paxillin mutants are significantly smaller overall. No obvious heart structure is present (Ht), and mutants have an abnormal headfold (Hf) and allantois (All). (E to H) Histological sections of wild-type and paxillin-null embryos. The headfold region is smaller than normal, but expected cell populations are present adjacent to the neural groove (NG), including neural epithelium (NE) and cephalic mesenchyme (CM). In contrast, the mutant embryo lacks a cardiogenic plate (CP) and the endodermal lining of the foregut (FG) remains open. The allantois (All) also appears to be abnormal. (G) A more caudal section of a wild-type embryo, in which the notochord (NC) and rostral extension of dorsal aorta (DA) are visible. Adjacent to the primitive streak (PS), mesodermal cells (M) are visible. (H) More caudal section of a paxillin-null embryo, in which the discrepancy in overall headfold size, compared to that of the wild type, is more pronounced. Cephalic mesenchymal (CM) cells appear condensed. Mutant embryos also lack an organized notochord, and the dorsal aorta is absent. Paxillin-null embryos also lack organized somites (in more caudal sections; not shown). In contrast, the primitive streak (PS) and adjacent mesodermal (M) cells appear normal.