title: Comparative analysis of the promoter regions and transcriptional start sites of mouse Ly49 genes.
abstract: 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 H 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 are heterogeneous for all of the genes examined, and that a large majority of Ly49G transcripts originate from the second exon 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.
authors.affiliation: Terry Fox Laboratory, BC Cancer Agency, Vancouver, Canada.
authors.forename: B T
authors.initials: BT
authors.lastname: Wilhelm
authors.forename: K L
authors.initials: KL
authors.lastname: McQueen
authors.forename: J D
authors.initials: JD
authors.lastname: Freeman
authors.forename: F
authors.initials: F
authors.lastname: Takei
authors.forename: D L
authors.initials: DL
authors.lastname: Mager
mesh_terms: D000818:Animals; D000950:Antigens, Ly; D001665:Binding Sites; D004268:DNA-Binding Proteins / Q000378:metabolism; D015870:Gene Expression; D006801:Humans; D037181:Lectins, C-Type; D051821:Lymphoid Enhancer-Binding Factor 1; D008562:Membrane Glycoproteins / Q000235:genetics*; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D055650:NK Cell Lectin-Like Receptor Subfamily A; D011401:Promoter Regions, Genetic; D011971:Receptors, Immunologic / Q000235:genetics*; D055630:Receptors, NK Cell Lectin-Like; D012045:Regulatory Sequences, Nucleic Acid; D017422:Sequence Analysis, DNA; D012689:Sequence Homology, Nucleic Acid; D016385:TATA Box; D014157:Transcription Factors / Q000378:metabolism; D014158:Transcription, Genetic
chemical_list: D000950:Antigens, Ly; D004268:DNA-Binding Proteins; C527090:Klra2 protein, mouse; C527095:Klra7 protein, mouse; D037181:Lectins, C-Type; D051821:Lymphoid Enhancer-Binding Factor 1; D008562:Membrane Glycoproteins; D055650:NK Cell Lectin-Like Receptor Subfamily A; D011971:Receptors, Immunologic; D055630:Receptors, NK Cell Lectin-Like; D014157:Transcription Factors