AML1(-/-) embryos do not express certain hematopoiesis-related gene transcripts including those of the PU.1 gene
AML1(-/-) embryos do not express certain hematopoiesis-related gene transcripts including those of the PU.1 gene
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DOI：
10.1038/sj.onc.1202151
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发表时间：
1998-11-05
期刊：
影响因子：
8
通讯作者：
Satake, M
中科院分区：
文献类型：
--
作者：
Okada, H;Watanabe, T;Satake, M
AML 1和PEBP 2 β/CBF β基因分别编码异二聚体转录因子PEBP 2/CBF的DNA结合和非结合亚基。靶向每个基因导致几乎相同的表型，即在胚胎第11.5天（E11.5）的胎儿肝脏中完全缺乏确定的造血。我们检查并比较了野生型胚胎和AML 1或PEBP 2 β/CBF β突变胚胎中各种造血相关基因的表达水平。从E9.5胚胎的卵黄囊、E11.5胚胎的卵黄囊-性腺-中肾区和E11.5胚胎的肝脏中制备RNA，并进行RT-PCR以检测各种基因转录本。转录本中检测到的大多数造血相关基因编码转录因子，细胞因子和细胞因子受体，甚至在组织同源靶向胚胎。另一方面，在AML 1（-/-）或PEBP 2 β/CBF β（-/-）胚胎的任何组织中从未检测到PU.1转录本。此外，在（-/-）胚胎的某些组织中未检测到Vav、flk-2/flt-3、M-CSF受体、G-CSF受体和c-Myb基因的转录物。结果表明，一组特定的造血相关基因的表达与PEBP 2/CBF功能密切相关。
The AML1 and PEBP2 beta/CBF beta genes encode the DNA-binding and non-binding subunits, respectively, of the heterodimeric transcription factor, PEBP2/CBF. Targeting each gene results in an almost identical phenotype, namely the complete lack of definitive hematopoiesis in the fetal liver on embryonic day 11.5 (E11.5). We examined and compared the expression levels of various hematopoiesis-related genes in wild type embryos and in embryos mutated for AML1 or PEBP2 beta/CBF beta. The RNAs were prepared from the yolk sacs of E9.5 embryos, from the aorta-gonad- mesonephros regions of E11.5 embryos and from the livers of E11.5 embryos and RT-PCR was performed to detect various gene transcripts. Transcripts were detected for most of the hematopoiesis-related genes that encode transcription factors, cytokines and cytokine receptors, even in tissues from homozygously targeted embryos. On the other hand, PU.1 transcripts were never detected in any tissue of AML1(-/-) or PEBP2 beta/CBF beta(-/-) embryos. In addition, transcripts for the Vav, flk-2/flt-3, M-CSF receptor, G-CSF receptor and c-Myb genes were not detected in certain tissues of the (-/-) embryos. The results suggest that the expression of a particular set of hematopoiesis-related genes is closely correlated with the PEBP2/CBF function.