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SCL基因产物：红细胞分化的正向调节因子。

The SCL gene product: a positive regulator of erythroid differentiation.

作者信息

Aplan P D, Nakahara K, Orkin S H, Kirsch I R

机构信息

National Cancer Institute, Navy Medical Branch, Bethesda, MD 20889.

出版信息

EMBO J. 1992 Nov;11(11):4073-81. doi: 10.1002/j.1460-2075.1992.tb05500.x.

DOI:10.1002/j.1460-2075.1992.tb05500.x
PMID:1396592
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC556917/
Abstract

The SCL (tal-1, TCL5) gene is a member of the basic domain, helix-loop-helix (bHLH) class of putative transcription factors. We found that (i) the SCL promoter for exon Ia contains a potential recognition site for GATA-binding transcription factors, (ii) SCL mRNA is expressed in all erythroid tissues and cell lines examined, and (iii) SCL mRNA increases upon induced differentiation of murine erythroleukemia (MEL) cells, and inferred that SCL may play a physiologic role in erythroid differentiation. We used gel shift and transfection assays to demonstrate that the GATA motif in the SCL promoter binds GATA-1 (and GATA-2), and also mediates transcriptional transactivation. To identify a role for SCL in erythroid differentiation, we generated stable transfectants of MEL and K562 (a human chronic myelogenous leukemia cell line that can differentiate along the erythroid pathway) cells overexpressing wild-type, antisense or mutant SCL cDNA. Increasing the level of SCL expression in two independent MEL lines (F4-6 and C19, a 745 derivative) and K562 cells increased the rate of spontaneous (i.e. in the absence of inducer) erythroid differentiation. Conversely, induced differentiation was inhibited in MEL transfectants expressing either antisense SCL cDNA or a mutant SCL lacking the basic domain. Our experiments suggest that the SCL gene can be a target for the erythroid transcription factor GATA-1 and that the SCL gene product serves as a positive regulator of erythroid differentiation.

摘要

SCL（tal-1，TCL5）基因是假定转录因子的碱性结构域、螺旋-环-螺旋（bHLH）类成员。我们发现：（i）外显子Ia的SCL启动子含有一个GATA结合转录因子的潜在识别位点；（ii）SCL mRNA在所检测的所有红系组织和细胞系中均有表达；（iii）SCL mRNA在小鼠红白血病（MEL）细胞诱导分化时增加，并推断SCL可能在红系分化中发挥生理作用。我们使用凝胶迁移和转染试验证明SCL启动子中的GATA基序结合GATA-1（和GATA-2），并介导转录反式激活。为了确定SCL在红系分化中的作用，我们构建了过表达野生型、反义或突变型SCL cDNA的MEL和K562（一种可沿红系途径分化的人慢性髓性白血病细胞系）细胞的稳定转染子。在两个独立的MEL细胞系（F4-6和C19，一种745衍生物）和K562细胞中增加SCL表达水平，可提高自发（即在无诱导剂情况下）红系分化的速率。相反，在表达反义SCL cDNA或缺乏碱性结构域的突变型SCL的MEL转染子中，诱导分化受到抑制。我们的实验表明，SCL基因可能是红系转录因子GATA-1的作用靶点，并且SCL基因产物作为红系分化的正调节因子。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9490/556917/88624c526c53/emboj00096-0266-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9490/556917/4aa7b700e037/emboj00096-0262-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9490/556917/416199eff9d0/emboj00096-0263-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9490/556917/4389ae5eaca2/emboj00096-0264-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9490/556917/41f00485240c/emboj00096-0265-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9490/556917/88624c526c53/emboj00096-0266-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9490/556917/4aa7b700e037/emboj00096-0262-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9490/556917/416199eff9d0/emboj00096-0263-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9490/556917/4389ae5eaca2/emboj00096-0264-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9490/556917/41f00485240c/emboj00096-0265-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9490/556917/88624c526c53/emboj00096-0266-a.jpg

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