CLONING AND CHARACTERIZATION OF AN ATBF1 ISOFORM THAT EXPRESSES IN A NEURONAL DIFFERENTIATION-DEPENDENT MANNER
CLONING AND CHARACTERIZATION OF AN ATBF1 ISOFORM THAT EXPRESSES IN A NEURONAL DIFFERENTIATION-DEPENDENT MANNER
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DOI：
10.1074/jbc.270.45.26840
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发表时间：
1995-11-10
影响因子：
4.8
通讯作者：
TAMAOKI, T
中科院分区：
文献类型：
--
作者：
MIURA, Y;TAM, T;TAMAOKI, T
以前报道的人类ATBF1基因，现在被命名为ATBF1-B，编码一个306 kDa的蛋白，包含4个同源结构域和18个锌指，其中包括一个假锌指基序。推导的ATBF1-A蛋白全长404 kDa，N端与ATBF1-B相差920个氨基酸。5‘-基因组序列分析表明，ATBF1-A和ATBF1-B转录本的5’-非编码序列位于不同的外显子中，该外显子可与ATBF1-A和ATBF1-B mRNAs的下游外显子拼接。用维甲酸诱导P19和NT2/D1细胞分化时，ATBF1-A基因转录产物表达水平升高。在发育中的小鼠脑中也观察到ATBF1-A转录本的分化、优先表达。瞬时转染实验表明，ATBF1-A特异性外显子(外显子2)上游的5，5千碱基序列支持连接的氯霉素乙酰转移酶基因在P19细胞来源的神经细胞中表达，但在未分化的P19细胞或F9细胞中不表达，后者不能分化为神经元。这些结果表明，ATBF1-A和ATBF1-B转录本是通过交替使用启动子和选择性剪接产生的，并且ATBF1-A特异性启动子在神经元分化过程中被激活。
The human ATBF1 cDNA reported previously, now termed ATBF1-B, encodes a 306-kDa protein containing 4 homeodomains and 18 zinc fingers including one pseudo zinc finger motif, Here, we report the isolation of a second ATBF1 cDNA, 12 kilobase pairs long, termed ATBF1-A. The deduced ATBF1-A protein is 404 kDa in size and differs from ATBF1-B by a 920-amino acid extention at the N terminus, Analysis of 5'-genomic sequences showed that the 5'-noneoding sequences specific to ATBF1-A and ATBF1-B transcripts were contained in distinct exons that could splice to a downstream exon common to the ATBF1-A and ATBF1-B mRNAs. The expression of ATBF1-A transcripts increased to high levels when P19 and NT2/D1 cells were treated with retinoic acid to induce neuronal. differentiation, Preferential expression of ATBF1-A transcripts was also observed in developing mouse brain. Transient transfection assays showed that the 5,5-kilobase pair sequence upstream of the ATBF1-A-specific exon (exon 2) supported expression of the linked chloramphenicol acetyltransferase gene in neuronal cells derived from P19 cells but not in undifferentiated P19 or in F9 cells, which do not differentiate into neurons. These results showed that ATBF1-A and ATBF1-B transcripts are generated by alternative promoter usage combined with alternative splicing and that the ATBF1-A-specific promoter is activated during neuronal differentiation.