Fig. 6. In situ hybridization analysis of the paraxial mesoderm marker Mox1 indicates a defect in expression maintenance in Mll2^–/– mutant embryos. Whole-mount embryos (A-D) and transverse sections (E-G) are depicted. (A) Expression of Mox1 in the presomitic mesoderm and somites of an E8.4 wild-type embryo (eight somites). (B) Expression of Mox1 in an E9.0 Mll2^–/– embryo with eight somites. (C) In an E9.5 Mll2^–/– embryo with 10 somites, Mox1 expression was lost in the anterior somites. (D) In an E9.75 Mll2^–/– embryo, almost no Mox1 expression was detected. Defective longitudinal extension of paraxial mesoderm is the most likely cause of the uneven and compressed shape of the neural tube in mutant embryos at this stage. (E) Transverse section of the E8.4 wild-type embryo displayed in A shows mox1 expression in paraxial mesoderm. (F) TUNEL stained transverse section of the E9.5 Trx2^–/– embryo displayed in C. Only a few apoptotic nuclei appear throughout the section; therefore, the Mox1 signal (arrow) is not decreasing because of apoptosis of the entire paraxial mesoderm at this stage. (G) TUNEL-stained transverse section of an E10.5 Mll^–/– embryo. At this stage, the entire embryo section is positively stained, with the highest amount of apoptotic cells in the paraxial mesoderm (arrow).