Retarded postimplantation development of XO mouse embryos: Impact of the parental origin of the monosomic X chromosome

Retarded postimplantation development of XO mouse embryos: Impact of the parental origin of the monosomic X chromosome
复制标题

DOI:
10.1006/dbio.1998.8972
复制
发表时间:
1998-09-01
影响因子:
2.7
通讯作者:
Tam, PPL
Tam, PPL
中科院分区:
生物学3区
文献类型:
--
作者:
Jamieson, RV;Tan, SS;Tam, PPL

文献摘要

被引文献

相似文献

通过携带In(X)1H或Paf突变的小鼠交配获得的胚胎中约有12-17%是39,X(X 0)基因型。根据用于交配的突变小鼠,单体X染色体可以从父系(X-P)或母系(X-M)亲本遗传。X(P)0胚胎在原肠胚形成和早期器官发生时发育迟缓。X(P)0胚胎也显示外胎盘锥发育不良,与XX同胞相比,外胎盘锥明显较小,滋养层细胞较少。相比之下,X(M)0胚胎发育正常,与XX同窝仔难以区分。在这两种类型的X 0胚胎中,X连锁lacZ转基因在胚胎和胚外组织中的几乎所有细胞中表达,这表明当仅存在一个X时不会发生X失活。特别重要的是在胚外组织中维持活性X-P染色体,通常父方X染色体在XX胚胎中优先失活。来自不同亲本的X染色体的遗传对X 0胚胎发育的差异性影响提出了这样的可能性,即X-P在提供适当剂量的X连锁活性方面的能力低于X-M,所述适当剂量的X连锁活性是支持胚胎和外胎盘锥正常发育所必需的。或者,X(P)0胚胎的发育可能由于一个或几个仅从母体X染色体表达的X连锁基因缺乏活性而受到损害。如果没有这些基因的活性,即使X-P染色体上的所有其他位点都被活跃地转录,胚胎发育也可能被缩短。(C)北京:科学出版社.
About 12-17% of the embryos obtained by mating mice carrying the In(X)1H or Paf mutations are of the 39,X (X0) genotype. Depending on the mutant mice used for mating, the monosomic X chromosome can be inherited from the paternal (X-P) Or the maternal (X-M) parent. The X(P)0 embryos display developmental retardation at gastrulation and early organogenesis. X(P)0 embryos also display poor development of the ectoplacental cone, which is significantly smaller in size and contains fewer trophoblasts than XX siblings. In contrast, X(M)0 embryos develop normally and are indistinguishable from XX littermates. In both types of X0 embryos, an X-linked lacZ transgene is expressed in nearly all cells in both the embryonic and the extraembryonic tissues, suggesting that X inactivation does not occur when only one X is present. Of particular significance is the maintenance of an active X-P chromosome in the extraembryonic tissues where normally the paternal X chromosome is preferentially inactivated in XX embryos. The differential impact of the inheritance of X chromosomes from different parents on the development of the X0 embryos raises the possibility that the X-P is less capable than the X-M in providing the appropriate dosage of X-linked activity that is necessary to support normal development of the embryo and the ectoplacental cone. Alternatively, the development of the X(P)0 embryo may be compromised by the lack of activity of one or several X-linked genes which are expressed only from the maternal X chromosome. Without the activity of these genes, embryonic development may be curtailed even though all other loci on the X-P chromosome are actively transcribed. (C) 1998 Academic Press.