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小鼠T相关母体效应(Tme)基因座上基因组印记的逃逸。

Escape from genomic imprinting at the mouse T-associated maternal effect (Tme) locus.

作者信息

Tsai J Y, Silver L M

机构信息

Department of Molecular Biology, Princeton University, New Jersey 08544-1014.

出版信息

Genetics. 1991 Dec;129(4):1159-66. doi: 10.1093/genetics/129.4.1159.

Abstract

Genomic imprinting occurs at the paternally inherited allele of the mouse T-associated maternal effect (Tme) locus. As a consequence, maternal transmission of a functional Tme gene is normally required for viability and individuals that receive a Tme-deleted chromosome (Thp or tlub2) from their mother die late in gestation or shortly thereafter. Here we report that a rearranged paternally derived chromosome duplicated for the Tme locus can act to rescue animals that have not received a maternal copy of the Tme locus. Unexpectedly, all rescued animals display an abnormal short/kinky tail phenotype. Somatic transfer of genomic imprinting between homologs by means of a transvection-like process between paired Tme and T loci is proposed as a model to explain the results obtained.

摘要

基因组印记发生在小鼠T相关母体效应(Tme)基因座的父系遗传等位基因上。因此,功能性Tme基因的母系传递通常是个体存活所必需的,那些从母亲那里获得Tme缺失染色体(Thp或tlub2)的个体在妊娠后期或之后不久死亡。在此,我们报告,一条为Tme基因座重复的重排父源染色体能够挽救那些未从母亲那里获得Tme基因座母本拷贝的动物。出乎意料的是,所有获救动物都表现出异常的短尾/卷曲尾表型。我们提出通过配对的Tme和T基因座之间类似转座的过程在同源染色体之间进行基因组印记的体细胞转移,作为解释所得结果的一种模型。

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Two doses of the paternal Tme gene do not compensate the lethality of the Thp deletion.
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Tcp-1 gene is not responsible for the maternal lethality effect of Thp mutation in mice.
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