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维甲酸诱导的小鼠脊柱裂中基因-致畸剂相互作用及其形态学基础

Gene-teratogen interaction and its morphological basis in retinoic acid-induced mouse spina bifida.

作者信息

Kapron-Brás C M, Trasler D G

出版信息

Teratology. 1984 Aug;30(1):143-50. doi: 10.1002/tera.1420300118.

DOI:10.1002/tera.1420300118
PMID:6385329
Abstract

Homozygotes for the splotch (Sp) mutation in the mouse have spina bifida, whereas the heterozygotes have a white belly spot but otherwise appear normal. Spina bifida can be induced by maternal treatment with retinoic acid. Female SWV strain mice were treated intraperitoneally with retinoic acid suspended in peanut oil 8 days/12 hours after they had been mated to either Sp/+ or +/+ males. Probit analysis of the dose-response data suggests that the presence of the Sp gene causes an increased susceptibility of the embryo to the spina bifida-causing effects of retinoic acid. To study the nature of this increase litters were obtained on gestation day 9 from untreated SWV females mated as above. The mean length of the posterior neuropore (the length of the posterior neural tube that has not yet closed) was determined for each somite number between 14 and 26 and was found to be significantly greater in embryos from the Sp/+ cross. This delay of closure of the neural tube in Sp/+ cross embryos could explain the observed increase in their susceptibility to retinoic acid.

摘要

小鼠中斑点(Sp)突变的纯合子患有脊柱裂,而异合子有白色腹部斑点,但其他方面看起来正常。脊柱裂可由母体用视黄酸治疗诱发。雌性SWV品系小鼠在与Sp/+或+/+雄性交配后8天/12小时,腹腔注射悬浮在花生油中的视黄酸。剂量反应数据的概率分析表明,Sp基因的存在会使胚胎对视黄酸导致脊柱裂的作用敏感性增加。为了研究这种增加的性质,在妊娠第9天从未经处理的如上所述交配的SWV雌性小鼠获得窝仔。确定了14至26之间每个体节数的后神经孔平均长度(尚未闭合的后神经管长度),发现Sp/+杂交的胚胎中该长度明显更长。Sp/+杂交胚胎中神经管闭合的延迟可以解释观察到的它们对视黄酸敏感性的增加。

相似文献

1
Gene-teratogen interaction and its morphological basis in retinoic acid-induced mouse spina bifida.维甲酸诱导的小鼠脊柱裂中基因-致畸剂相互作用及其形态学基础
Teratology. 1984 Aug;30(1):143-50. doi: 10.1002/tera.1420300118.
2
Early morphological abnormalities in splotch mouse embryos and predisposition to gene- and retinoic acid-induced neural tube defects.斑点小鼠胚胎的早期形态学异常以及对基因和视黄酸诱导的神经管缺陷的易感性。
Teratology. 1983 Dec;28(3):461-72. doi: 10.1002/tera.1420280318.
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Interaction between the splotch mutation and retinoic acid in mouse neural tube defects in vitro.体外研究斑点突变与视黄酸在小鼠神经管缺陷中的相互作用
Teratology. 1988 Aug;38(2):165-73. doi: 10.1002/tera.1420380209.
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Histological comparison of the effects of the splotch gene and retinoic acid on the closure of the mouse neural tube.斑点基因和视黄酸对小鼠神经管闭合影响的组织学比较
Teratology. 1988 Apr;37(4):389-99. doi: 10.1002/tera.1420370412.
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Studies of the effect of retinoic acid on anterior neural tube closure in mice genetically liable to exencephaly.视黄酸对易患无脑畸形的小鼠前神经管闭合影响的研究。
Teratology. 1991 Jan;43(1):27-40. doi: 10.1002/tera.1420430105.
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Reduction in the frequency of neural tube defects in splotch mice by retinoic acid.视黄酸降低斑点小鼠神经管缺陷的发生率。
Teratology. 1985 Aug;32(1):87-92. doi: 10.1002/tera.1420320112.
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Quantification and localization of expression of the retinoic acid receptor-beta and -gamma mRNA isoforms during neurulation in mouse embryos with or without spina bifida.有或没有脊柱裂的小鼠胚胎神经管形成过程中视黄酸受体β和γ mRNA亚型表达的定量与定位
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Gene-teratogen interaction in insulin-induced mouse exencephaly.胰岛素诱导的小鼠无脑畸形中的基因-致畸剂相互作用。
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Discontinuity of primary and secondary neural tube in spina bifida induced by retinoic acid in mice.维甲酸诱导的小鼠脊柱裂中初级和次级神经管的连续性中断。
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引用本文的文献

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Effect of infection with the ts22 mutant of Semliki Forest virus on development of the central nervous system in the fetal mouse.感染Semliki森林病毒ts22突变体对胎鼠中枢神经系统发育的影响。
J Virol. 1989 Sep;63(9):4027-33. doi: 10.1128/JVI.63.9.4027-4033.1989.
2
Splotch locus mouse mutants: models for neural tube defects and Waardenburg syndrome type I in humans.斑点基因座小鼠突变体:人类神经管缺陷和I型瓦登伯革氏综合征的模型
J Med Genet. 1992 Mar;29(3):145-51. doi: 10.1136/jmg.29.3.145.