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Cx31和Cx43双缺陷小鼠揭示了其在小鼠胎盘和皮肤发育中的独立功能。

Cx31 and Cx43 double-deficient mice reveal independent functions in murine placental and skin development.

作者信息

Kibschull Mark, Magin Thomas M, Traub Otto, Winterhager Elke

机构信息

Institute of Anatomy, University Hospital Duisburg-Essen, Essen, Germany.

出版信息

Dev Dyn. 2005 Jul;233(3):853-63. doi: 10.1002/dvdy.20424.

DOI:10.1002/dvdy.20424
PMID:15895417
Abstract

The overlapping expression of gap junctional connexins in tissues has indicated that the channels may compensate for each other. During development, Cx31 and Cx43 are coexpressed in preimplantation embryos, in the spongiotrophoblast of the placenta and in the epidermis. This study shows that Cx31/Cx43 double-deficient mice exhibit the known phenotypes of the single-knockout strains but no combined effects. Thus, Cx43, coexpressed with Cx31 at midgestation in the spongiotrophoblast of the placenta, cannot be responsible for a partial rescue of the lethal Cx31 knockout phenotype, as assumed before (Plum et al. [2001] Dev Biol 231:334-337). It follows that both connexins have unique functions in placental development. Despite an altered expression of other epidermal connexin mRNAs, epidermal differentiation and physiology was unaltered by the absence of Cx31 and Cx43. Therefore, in epidermal and preimplantation development, gap junctional communication can probably be compensated by other isoforms coexpressed with Cx31 and Cx43.

摘要

组织中缝隙连接蛋白的重叠表达表明这些通道可能相互补偿。在发育过程中,Cx31和Cx43在植入前胚胎、胎盘的海绵滋养层细胞和表皮中共同表达。本研究表明,Cx31/Cx43双缺陷小鼠表现出已知的单基因敲除品系的表型,但没有联合效应。因此,在妊娠中期与Cx31共同表达于胎盘海绵滋养层细胞中的Cx43,并不像之前所假设的那样(Plum等人,[2001]《发育生物学》231:334 - 337),对致死性Cx31基因敲除表型的部分挽救负责。由此可见,这两种连接蛋白在胎盘发育中具有独特的功能。尽管其他表皮连接蛋白mRNA的表达发生了改变,但表皮分化和生理功能并未因Cx31和Cx43的缺失而改变。因此,在表皮和植入前发育过程中,缝隙连接通讯可能由与Cx31和Cx43共同表达的其他异构体进行补偿。

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Cx31 and Cx43 double-deficient mice reveal independent functions in murine placental and skin development.Cx31和Cx43双缺陷小鼠揭示了其在小鼠胎盘和皮肤发育中的独立功能。
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