Hou Wenyang, Jerome-Majewska Loydie A
Department of Human Genetics, McGill University, 1205 Avenue Docteur Penfield, N5/13, Montreal, QC, Canada.
Department of Human Genetics, McGill University, 1205 Avenue Docteur Penfield, N5/13, Montreal, QC, Canada; Department of Anatomy and Cell Biology, McGill University, Montreal, QC, Canada; Department of Pediatrics, McGill University, 1001 Decarie Blvd, EM02210, Montreal, QC, Canada H4A 3J1; McGill University Health Centre Glen Site, 1001 Decarie Blvd, EM0.2210, Montreal, QC, Canada H4A 3J1.
Dev Biol. 2018 Dec 1;444(1):20-32. doi: 10.1016/j.ydbio.2018.09.012. Epub 2018 Sep 17.
TMED2, a member of the transmembrane emp24 domain (TMED) family, is required for transport of cargo proteins between the ER and Golgi. TMED2 is also important for normal morphogenesis of mouse embryos and their associated placenta, and in fact Tmed2 homozygous mutant embryos arrest at mid-gestation due to a failure of placental labyrinth layer formation. Differentiation of the placental labyrinth layer depends on chorioallantoic attachment (contact between the chorion and allantois), and branching morphogenesis (mingling of cells from these two tissues). Since Tmed2 mRNA was found in both the chorion and allantois, and 50% of Tmed2 homozygous mutant embryos failed to undergo chorioallantoic attachment, the tissue-specific requirement of Tmed2 during placental labyrinth layer formation remained a mystery. Herein, we report differential localization of TMED2 protein in the chorion and allantois, abnormal ER retention of Fibronectin in Tmed2 homozygous mutant allantoises and cell-autonomous requirement for Tmed2 in the chorion for chorioallantoic attachment and fusion. Using an ex vivo model of explanted chorions and allantoises, we showed that chorioallantoic attachment failed to occur in 50% of samples when homozygous mutant chorions were recombined with wild type allantoises. Furthermore, though expression of genes associated with trophoblast differentiation was maintained in Tmed2 mutant chorions with chorioallantoic attachment, expression of these genes was attenuated. In addition, Tmed2 homozygous mutant allantoises could undergo branching morphogenesis, however the region of mixing between mutant and wild type cells was reduced, and expression of genes associated with trophoblast differentiation was also attenuated. Our data also suggest that Fibronectin is a cargo protein of TMED2 and indicates that Tmed2 is required cell-autonomously and non-autonomously in the chorion and the allantois for placental labyrinth layer formation.
跨膜emp24结构域(TMED)家族成员TMED2是货物蛋白在内质网和高尔基体之间运输所必需的。TMED2对小鼠胚胎及其相关胎盘的正常形态发生也很重要,事实上,Tmed2纯合突变胚胎由于胎盘迷路层形成失败而在妊娠中期停滞发育。胎盘迷路层的分化取决于绒毛膜尿囊附着(绒毛膜和尿囊之间的接触)以及分支形态发生(这两种组织的细胞混合)。由于在绒毛膜和尿囊中都发现了Tmed2 mRNA,并且50%的Tmed2纯合突变胚胎未能进行绒毛膜尿囊附着,因此Tmed2在胎盘迷路层形成过程中的组织特异性需求仍是一个谜。在此,我们报告了TMED2蛋白在绒毛膜和尿囊中的差异定位,Tmed2纯合突变尿囊中纤连蛋白在内质网的异常滞留,以及绒毛膜中Tmed2对绒毛膜尿囊附着和融合的细胞自主需求。使用绒毛膜和尿囊外植体的体外模型,我们发现当纯合突变绒毛膜与野生型尿囊重组时,50%的样本未能发生绒毛膜尿囊附着。此外,尽管在具有绒毛膜尿囊附着的Tmed2突变绒毛膜中与滋养层分化相关的基因表达得以维持,但这些基因的表达减弱。此外,Tmed2纯合突变尿囊可以进行分支形态发生,然而突变细胞与野生型细胞之间的混合区域减少,并且与滋养层分化相关的基因表达也减弱。我们的数据还表明纤连蛋白是TMED2的货物蛋白,并表明Tmed2在绒毛膜和尿囊中对胎盘迷路层形成具有细胞自主和非自主需求。