Johnston J J, Rintels P, Chung J, Sather J, Benz E J, Berliner N
Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06510.
Blood. 1992 Jun 1;79(11):2998-3006.
Lactoferrin is a member of the transferrin family of iron-binding proteins. It is found in several glandular epithelial tissues and human neutrophils, where it is localized to secondary granules. To examine the mechanisms controlling lactoferrin gene expression in neutrophils and defects in its expression in acute leukemia, we have cloned a lactoferrin cDNA from a chronic myelogenous leukemia library, and used it to obtain genomic clones representing the chromosomal lactoferrin gene. Using polymerase chain reaction, primer extension, and S1 analysis, we have identified the 5' end of the lactoferrin mRNA. We have defined a putative promoter region for the gene, and characterized its first two exons. In addition, we have examined the structure of these regions in DNA from HL60 cells. HL60 is a leukemic cell line that undergoes phenotypic neutrophil maturation on exposure to dimethyl sulfoxide (DMSO). However, the cells cannot be induced to express any secondary granule protein genes. We have shown that the 5' end of the lactoferrin gene, including the putative promoter region, is entirely normal in HL60. By Northern analysis, nuclear run-on studies, and primer extension assays we have shown that the gene is not transcribed in DMSO-induced HL60 cells. This supports the hypothesis that the defect in HL60 is an abnormality in the production or activity of a transacting regulator of lactoferrin gene expression.
乳铁蛋白是铁结合蛋白转铁蛋白家族的成员。它存在于几种腺上皮组织和人类中性粒细胞中,定位于次级颗粒。为了研究控制中性粒细胞中乳铁蛋白基因表达的机制及其在急性白血病中表达的缺陷,我们从慢性粒细胞白血病文库中克隆了乳铁蛋白cDNA,并利用它获得了代表染色体乳铁蛋白基因的基因组克隆。通过聚合酶链反应、引物延伸和S1分析,我们确定了乳铁蛋白mRNA的5'端。我们定义了该基因的一个假定启动子区域,并对其前两个外显子进行了特征分析。此外,我们还研究了HL60细胞DNA中这些区域的结构。HL60是一种白血病细胞系,在接触二甲基亚砜(DMSO)时会经历表型中性粒细胞成熟。然而,这些细胞不能被诱导表达任何次级颗粒蛋白基因。我们已经证明,HL60中乳铁蛋白基因的5'端,包括假定的启动子区域,完全正常。通过Northern分析、核转录分析和引物延伸试验,我们已经证明该基因在DMSO诱导的HL60细胞中不转录。这支持了这样一种假设,即HL60中的缺陷是乳铁蛋白基因表达的反式作用调节因子的产生或活性异常。