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首页> 外文期刊>Genomics >Bidirectional transcriptional activity of the Pgk1 promoter and transmission ratio distortion in Capn3-deficient mice.
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Bidirectional transcriptional activity of the Pgk1 promoter and transmission ratio distortion in Capn3-deficient mice.

机译：Capg3缺陷小鼠中Pgk1启动子的双向转录活性和传输比畸变。

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A calpain 3 (Capn3) deficiency model was created by targeted disruption of the mouse Capn3 gene through homologous recombination in ES cells. Analysis of the genotype of pups from heterozygous crosses revealed a transmission ratio distortion (TRD) in favor of homozygous Capn3-deficient mice. This TRD was not observed in a second model of Capn3 deficiency, ruling out a possible involvement of Capn3 deficiency in this phenotype. The molecular nature of the TRD was investigated by quantitative RT-PCR and RACE-PCR analyses. We observed the presence in testis and ovaries of abundant, novel transcripts of the Capn3 gene arising from the antisense strand of the Pgk1-neomycin cassette. Although we could not detect corresponding translation products, our results suggest that the activity of the Pgk1 promoter could be the causative factor of TRD. This first example of TRD induced by an introduced cassette further emphasizes the care that should be taken in interpreting phenotypes of animal models, especially when dealing with reproductive functions, and further supports the rationale of using excisable cassettes in inactivation strategies.
机译：通过在ES细胞中通过同源重组靶向破坏小鼠Capn3基因来创建钙蛋白酶3（Capn3）缺乏模型。对来自杂合子杂交的幼犬的基因型的分析表明，有一个纯合的Capn3缺陷型小鼠有利于传播比率失真（TRD）。在第二个Capn3缺乏症模型中未观察到该TRD，排除了Capn3缺乏症可能与该表型有关。通过定量RT-PCR和RACE-PCR分析研究TRD的分子性质。我们观察到在睾丸和卵巢中存在大量的，源自Pgk1-neomycin盒反义链的Capn3基因的新颖转录本。尽管我们无法检测到相应的翻译产物，但我们的结果表明Pgk1启动子的活性可能是TRD的致病因素。由引入的盒引起的TRD的第一个例子进一步强调了在解释动物模型表型时应特别注意的问题，特别是在处理生殖功能时，并进一步支持在灭活策略中使用可切除盒的原理。

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