The early embryonic expression of TFII-I during mouse preimplantation development

The early embryonic expression of TFII-I during mouse preimplantation development
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DOI:
10.1016/s1567-133x(03)00155-8
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发表时间:
2004-01-01
影响因子:
1.2
通讯作者:
Bayarsaihan, DZ
Bayarsaihan, DZ
中科院分区:
生物学4区
文献类型:
--
作者:
Enkhmandakh, B;Bitchevaia, N;Bayarsaihan, DZ

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我们研究了小鼠TFII-I的发育调控表达,TFII-I是转录因子家族的创始成员,其特征在于存在多个螺旋-环-螺旋重复结构域。TFII-I和BEN是该家族的第二个成员,参与组蛋白修饰和SUMO化。编码这些蛋白质的基因GTF 2 I和GTF 2 IRD 1位于染色体7q11.23,在威廉姆斯综合征的关键区域内。我们的免疫组化分析显示广泛的TFII-I表达在胚胎发生的早期阶段。像BEN一样,TFII-I在受精后至第一卵裂期胚胎的细胞质和细胞核中检测到。然而,在E4.5囊胚中,在植入时,TFII-I定位于内细胞团(ICM)和滋养外胚层的细胞核和细胞质中。在此阶段,BEN仅在滋养层细胞的细胞质中表达,而不在ICM中表达[Gene Expr. Patterns,2003; 3,577-587]。采用RT-PCR方法检测未受精卵中Gtf 2 i和Gtf 2 ird 1的mRNA转录水平,表明这些基因在母体中表达。因此,TFII-I的早期胚胎表达暗示了这个转录因子家族在植入前发育中的作用。(C)2003 Elsevier B. V.保留所有权利。
We studied the developmentally regulated expression of mouse TFII-I, a founding member of a family of transcription factors characterized by the presence of multiple helix-loop-helix repeat domains. TFII-I and BEN, a second member of this family, are involved in histone modification and SUMOylation. The genes, GTF2I and GTF2IRD1, encoding these proteins in human are located at chromosomal band 7q11.23, within the Williams syndrome critical region. Our immunohistochemical analysis revealed extensive expression of TFII-I at early stages of embryogenesis. Like BEN, TFII-I is detected in the cytoplasm and nuclei of postfertilization through first cleavage stage embryos. However, in E4.5 blastocysts, at the time of implantation, TFII-I is localized in the nucleus and cytoplasm of the inner cell mass (ICM) and trophectoderm. BEN, at this stage, is expressed only in the cytoplasm of trophoblast cells, but not in the ICM [Gene Expr. Patterns, 2003; 3, 577-587]. Using RT-PCR, we detected Gtf2i and Gtf2ird1 mRNA transcripts in unfertilized oocytes, which indicates the maternal expression of these genes. Thus, the early embryonic expression of TFII-I implicates this family of transcription factors in preimplantation development. (C) 2003 Elsevier B.V. All rights reserved.