By Sabine Globig
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Reece EA, Wu YK: Prevention of diabetic embryopathy in offspring of diabetic rats with use of a cocktail of deficient substrates and an antioxidant. Am J Obstet Gynecol 1997, 176(4):790–797. 46 Current Research in Embryology 48. Wentzel P, Gareskog M, Eriksson UJ: Folic acid supplementation diminishes diabetes- and glucose-induced dysmorphogenesis in rat embryos in vivo and in vitro. Diabetes 2005, 54(2):546–553. 49. Pickett EA, Olsen GS, Tallquist MD: Disruption of PDGFRalpha-initiated PI3K activation and migration of somite derivatives leads to spina bifida.
Figure 1. Immunohistochemistry of Hsp105 in rat uterus during early pregnancy. Hsp105 protein was observed mainly in the luminal epithelium on day 1 of pregnancy (D1) and moderately expressed in the luminal epithelium and the glandular epithelium from day 2 to day 3 (D2). Hsp105 staining was also detected in the stromal cells, immediately underneath the luminal epithelium on day 4 and day 5 of pregnancy (D4, D5), the staining was increased markedly on day 5 just before implantation (D5). On day 6, the protein staining was mainly observed in the implanted blastocyst and the stromal cells around the implantation site (D6), while its expression in the luminal epithelium reduced to an undetected level.
Annotation for function in vivo identified 1836 gene entries in MGI; for 1095 of those, phenotype information was not available. However, 747 genes were associated with documented phenotypes in mouse mutants, of which 388 are developmental phenotypes by virtue of embryonic, neonatal, or perinatal death of homozygous mutant offspring. Again, the distribution of particular phenotypes in Experiment II (Figure 3, Panel D) was very similar to that of Experiment I (Figure 3, Panel C). Metabolic abnormalities were reported for mutants of 46 genes, and evidence for abnormal growth (pre- and post-natal) was obtained for 279 genes.