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首页> 外文期刊>American Journal of Physiology >Early transcription from the maternal genome controlling blastomere integrity in mouse two-cell-stage embryos.
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Early transcription from the maternal genome controlling blastomere integrity in mouse two-cell-stage embryos.

机译：母本基因组的早期转录控制着小鼠两细胞期胚胎中的卵裂球完整性。

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Blastomere cytofragmentation in mammalian embryos poses a significant problem in applied and clinical embryology. Mouse two-cell-stage embryos display strain-dependent differences in the rate of cytofragmentation, with a high rate observed in C3H/HeJ embryos and a lower rate observed in C57BL/6 embryos. The maternally inherited genome exerts the strongest effect on the process, with lesser effects mediated by the paternally inherited genome and the ooplasm. The effect of the maternal genome is transcription dependent and independent of the mitochondrial strain of origin. To identify molecular mechanisms that underlie cytofragmentation, we evaluated transcriptional activities of embryos possessing maternal pronuclei (mPN) of different origins. The mPN from C57BL/6 and C3H/HeJ strains directed specific transcription at the two-cell stage of mRNAs corresponding to 935 and 864 Affymetrix probe set IDs, respectively. Comparing transcriptomes of two-cell-stage embryos with different mPN revealed 64 transcribed genes with differential expression (1.4-fold or greater). Some of these genes occupy molecular pathways that may regulate cytofragmentation via a combination of effects related to apoptosis and effects on the cytoskeleton. These results implicate specific molecular mechanisms that may regulate cytofragmentation in early mammalian embryos. The most striking effect of mPN strain of origin on gene expression was on adenylate cyclase 2 (Adcy2). Treatment with dibutyryl cAMP (dbcAMP) elicits a high rate and severe form of cytofragmentation, and the effective dbcAMP concentration varies with maternal genotype. An activator of exchange proteins directly activated by cAMP (EPACs, or RAPGEF 3 and 4) 8-pCPT-2'-O-methyl-cAMP, elicits a high level of fragmentation while the PKA-specific activator N6-benzoyl-cAMP does not. Inhibition of A kinase anchor protein activities with st-Ht31 induces fragmentation. Inhibition of phosphatidylinositol 3-kinase signaling also induces fragmentation. These results reveal novel mechanisms by which maternal genotype affects cytofragmentation, including a system of opposing signaling pathways that most likely operate by controlling cytoskeletal function.
机译：哺乳动物胚胎中的卵裂球细胞碎片化在应用和临床胚胎学中提出了重大问题。小鼠两细胞期胚胎在细胞碎片化率上显示出应变依赖性差异，在C3H / HeJ胚胎中观察到高比率，在C57BL / 6胚胎中观察到低比率。母本遗传的基因组对该过程发挥最强的作用，而父本遗传的基因组和卵质介导的作用较小。母体基因组的作用是转录依赖性的，并且与起源的线粒体菌株无关。为了确定构成细胞碎片基础的分子机制，我们评估了拥有不同来源母体前核（mPN）的胚胎的转录活性。来自C57BL / 6和C3H / HeJ菌株的mPN分别在对应于935和864 Affymetrix探针组ID的mRNA的两细胞阶段指导特异性转录。比较具有不同mPN的两细胞期胚胎的转录组，发现64种转录基因具有差异表达（1.4倍或更高）。这些基因中的一些占据分子途径，该分子途径可通过与凋亡相关的作用和对细胞骨架的作用的组合来调节细胞碎片化。这些结果暗示了可能调控早期哺乳动物胚胎中细胞碎片化的特定分子机制。 mPN起源菌株对基因表达的最显着影响是对腺苷酸环化酶2（Adcy2）的影响。用二丁酰cAMP（dbcAMP）进行治疗会引起高水平和严重的细胞碎片化，有效dbcAMP浓度随母体基因型而异。由cAMP（EPAC或RAPGEF 3和4）8-pCPT-2'-O-甲基-cAMP直接激活的交换蛋白激活剂引起高水平的片段化，而PKA特异性激活剂N6-苯甲酰基-cAMP不激活。 st-Ht31抑制A激酶锚蛋白的活性会诱导片段化。磷脂酰肌醇3-激酶信号转导的抑制也诱导片段化。这些结果揭示了母本基因型影响细胞碎片的新机制，包括最有可能通过控制细胞骨架功能起作用的相反信号通路的系统。

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