Comparative analysis of the promoter regions and transcriptional start sites of mouse Ly49 genes

被引:27
|
作者
Wilhelm, BT
McQueen, KL
Freeman, JD
Takei, F
Mager, DL
机构
[1] British Columbia Canc Agcy, Terry Fox Lab, Vancouver, BC V5Z 1L3, Canada
[2] Univ British Columbia, Dept Med Genet, Vancouver, BC V6T 1W5, Canada
[3] Univ British Columbia, Dept Pathol, Vancouver, BC V5Z 1M9, Canada
基金
英国医学研究理事会; 加拿大自然科学与工程研究理事会;
关键词
natural killer (NK) cell; Ly49; promoter; transcriptional initiation; gene regulation;
D O I
10.1007/s002510100313
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Despite numerous studies on the function of Ly49 natural killer cell receptors in the mouse, relatively little is known about how these genes are regulated at the transcriptional level. In the present study, we sequenced and compared 800 bp of the promoter region of nine Ly49 genes from C57B1/6 mice. This comparison showed that there is a high degree of sequence identity between the genes, and also revealed a region which is conserved between the mouse genes and the human Ly49L gene, indicating a potential core promoter region. This analysis also found that Ly49B and W differ from the other genes in having long interspersed repetitive sequence in their promoter region which suggests a gene conversion or rearrangement involving these two genes. In addition, we performed 5' rapid amplification of cDNA ends on four Ly49 genes to localize transcriptional start sites. These experiments showed that the transcriptional initiation sites art: heterogeneous for all of the genes examined, and that a large majority of Ly49G transcripts originate from the second exori as well as its first. intron. Although potential TATA boxes have been previously identified for some of the genes, we did not find evidence that a majority of transcripts initiate at the expected distance downstream of these boxes. Our data suggest that differences in the location of transcriptional start sites contribute to the observed complexity in receptor repertoire patterns.
引用
收藏
页码:215 / 224
页数:10
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