The developmental pathology of maternally derived Thp fetuses.
The developmental pathology of maternally derived Thp fetuses.
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母体 Thp 胎儿的发育病理学。
DOI：
10.1002/tera.1420370409
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发表时间：
1988
期刊：
影响因子：
--
通讯作者：
Hathaway,HJ
中科院分区：
文献类型：
--
作者：
Babiarz,BS;Donovan,MJ;Hathaway,HJ
Tharpin（Thp）突变是小鼠17号染色体上5厘摩的缺失。当突变染色体通过雌性传递给胎儿时，杂合子胎儿（Thp/+）在子宫内死亡。如果染色体通过男性，杂合子是可行的，并显示短尾表型。这些母体衍生的突变胚胎为研究不完整的雌性基因组对发育的影响提供了一个很好的模型系统。本文报告的结果描述了从发育至出生第14天受影响胎儿的病理学研究结果。这些观察结果表明，母体来源的胎儿死于子宫内的充血性心力衰竭。突变胎儿表现出心脏增大，主要是右侧，以及其他心血管异常，包括室间隔缺损、主动脉狭窄、肺动脉扩张和静脉循环系统扩张。胎仔还显示内脏卵黄囊和羊膜中胎外液异常积聚，以及大量皮下水肿和腹水。Thp胎儿通常是苍白和贫血的，他们表现出每单位体积血液中红细胞数量减少，循环中有核红细胞增加。还观察到胎盘的绒毛膜和海绵滋养层区域发育缺陷。对这些缺陷的发病机理进行了讨论。
TheThair pin(Thp) mutation is a deletion of 5 centimorgans of chromosome 17 in the mouse. When the mutant chromosome is passed to the fetus through the female, the heterozygous fetuses (Thp/+) die in utero. If the chromosome is passed through the male, the heterozygotes are viable and display a short‐tailed phenotype. These maternally derived mutant embryos provide an excellent model system to study the effects of an incomplete female genome on development. The results reported here describe the findings of a pathological study of the affected fetuses from day 14 of development to birth. These observations indicate that the maternally derivedThpfetuses die in utero of congestive heart failure. The mutant fetuses displayed an enlarged heart, primarily the right side, and other cardiovascular abnormalities including ventricular septal defects, aortic stenosis, pulmonary artery dilation, and dilation of the venous circulatory system. The fetuses also displayed abnormal accumulation of extrafetal fluid in the visceral yolk sac and amion, as well as massive subcutaneous edema and ascites. TheThpfetuses were often pale and anemic, and they showed a decreased number of red blood cells per unit volume of blood and an increase in circulating nucleated red blood cells. Defects in the development of the labyrinthine and spongiotrophoblast regions of the placenta were also observed. The pathogenesis of the defects is discussed.