tailieunhanh - Biochemical, Genetic, and Molecular Interactions in Development - part 9

Phân tích mô học của sinh bệnh học của midface các hàm ếch. Phần ngang qua Thủ trưởng 10,5 UBND huyện hoang dã loại (+/+), nam đồng hợp tử (Sp2H/Sp2H), và Patch đồng hợp tử (Ph / Ph) đột biến phôi. Mức 10,5 UBND huyện, tự nhiên loại túi (tele) telencephalic là còn nguyên vẹn trong khu vực trán | 342 Conway Fig. 3. Histological analysis of the pathogenesis of the midface cleft. Transverse sections through the heads of wild-type male homozygous Sp2H Sp2H and homozygous Patch Ph Ph mutant embryos. At dpc the wild-type telencephalic tele vesicle is intact within the forehead region and there is a large open chamber. The communication between the optic stalk and intra-retinal space is intact and there is space between the walls of the third ventricle plus the chamber of the fourth ventricle 4th Vent is intact. Note that while the Ph Ph mutant head is grossly normal at dpc the Sp2H Sp2H mutant head is already malformed. There is a large midface cleft indicated by the space of the telencephalon and third chamber is missing and the neuroepithelial walls of the telencephalon and third chamber abut each other. Also this embryo has exencephaly ex and the chamber of the fourth ventricle is lost. Bar mm. Fig. 4. Apoptotic cell death. TUNEL analysis in wild-type and homozygous Sp2H Sp2H mutant male embryos as detected by the whole death method. The wild-type embryo viewed frontally has a seam of apoptotic cells along the frontonasal region of the anterior neuropore indicated by arrowheads following fusion of the neural folds. Also note that there are normal levels of apoptosis within the heart h and in the remodeling somites. There are equivalent levels of apoptotic cells within both the Sp2H Sp2H mutant frontonasal regions even though one mutant middle embryo has a closed anterior neuropore and exencephaly ex whereas the other mutant right has an open anterior neuropore and a mid-face cleft indicated by . It is interesting to note that there are still apoptotic cells along the neural folds in the cleft-face mutant even in the absence of fusion. mouse mutant models 28 53 . In the absence of pronounced cell death it appears that retinoic acid can possibly produce deleterious effects on the precursors of craniofacial primordia such as the