Disease relevance of Allantois

• Developing allantois is a primary site of 2'-deoxycoformycin toxicity [1].

High impact information on Allantois

• Mash-2 transcripts are not found in primary and secondary giant cells, yolk sac or allantois at any post-implantation stage, and are present only transiently and at low levels in the embryo during gastrulation [2].
• Rather, previous genetic analysis in the mouse has shown that bone morphogenetic protein 4 (Bmp4) is required for the formation of both PGCs and allantois [3].
• We also show by reverse transcription-PCR that the allantois region expresses very early the GATA genes involved in hematopoiesis and some beta-globin chain genes [4].
• Loss of both dph3 alleles causes a general delay in embryonic development accompanied by lack of allantois fusion to the chorion and increased degeneration and necrosis in neural tubes and is not compatible with life beyond embryonic day 11 [5].
• Previous research has shown that Smad1 is important in the formation of the allantois, while Smad5 has been shown to be critical in the process of angiogenesis [6].

Biological context of Allantois

• The allantois appears to be a significant distribution space for AFP in early gestation [7].
• Expression of the c-fos proto-oncogene by ovine conceptuses was analyzed by Northern and slot blots and indirect immunohistofluorescence in relation to the expression of the embryonic interferon-alpha (oTP) during implantation. c-fos was expressed initially in the trophoblast, and then in the allantois, when this tissue began to develop (day 17) [8].

Anatomical context of Allantois

• Cells taken from the region of the allantois and primitive streak can form colonies on hydrophilic Teflon (DuPont, Wilmington, DE) foils precoated with collagen and fibronectin [9].
• Extra-embryonic structures exhibit a number of differentiation defects: no vasculogenesis occurs in yolk sac or allantois; chorioallantoic fusion fails; the amnion does not expand with the growth of the embryo, but misexpresses vascular and hematopoietic markers [10].
• Loss of Tbx4 blocks hindlimb development and affects vascularization and fusion of the allantois [11].
• Benzidine-staining in situ revealed that primitive erythroid cells were not identified in the allantois until 6-somite pairs when continuity between its vasculature and that of the yolk sac was first evident [12].
• Furthermore, synchronous grafting of donor yolk sac containing blood islands into blood islands of headfold-stage host conceptuses provided no evidence that the yolk sac contributes endothelial cells to the allantois [12].

Associations of Allantois with chemical compounds

• Ovine chorion, allantois, and amnion from days 23, 26, 28, 35, 45, 53, 62, and 72 and yolk sac from day 23 of pregnancy were isolated by dissection and cultured for 24 h in modified minimum essential medium in the presence of [35S] methionine to characterize in vitro synthesis and release of proteins [13].
• Premature maturational changes in T4 and T3 metabolism, very similar to those that occurred spontaneously in 19- and especially 20-day-old embryos, were induced within 2 days by the single injection of 200 microgram hydrocortisone onto the allantoic membrane of immature embryos [14].
• Fetal fluid concentrations of progestagens, oestrone sulphate and PGF were not related to maternal plasma levels and a sequestration of these hormones by the allantois is postulated [15].
• 2-methoxyestradiol (2ME2), an endogenous metabolite of estradiol, has been shown in the chick allantoic membrane model and the corneal micropocket assay to have antiangiogenic properties [16].
• It appears that the avian allantois, in addition to its role in respiration and urea disposal, also serves the instant CA removal from the circulation [17].

Gene context of Allantois

• In addition, the allantois of many Smad5 mutants is fused to the chorion, but is not well-elongated [18].
• In addition, Bmp8b homozygous null embryos on both genetic backgrounds have a short allantois, and this organ is missing in some more severe mutants [19].
• Smad1 mutant mice die at approximately 9.5 days postcoitum due to defects in allantois formation [20].
• Bmp2 homozygous embryos also have a short allantois and about 50% of them do not undergo normal chorioallantoic fusion [21].
• 5. At E8.5, HGFR mRNA was detected in the chorionic placenta, and HGF mRNA was detected in the allantois [22].

References