Comprehensive analysis of transcript start sites in Ly49 genes reveals an unexpected relationship with gene function and a lack of upstream promoters

  1. Lookup NU author(s)
  2. Dr Jonathan Aust
  3. Professor Colin Brooks
Author(s)Gays F, Koh AS, Mickiewicz KM, Aust JG, Brooks CG
Publication type Article
JournalPLoS One
Year2011
Volume6
Issue3
Pages
ISSN (electronic)1932-6203
Full text is available for this publication:
Comprehensive analysis of the transcription start sites of the Ly49 genes of C57BL/6 mice using the oligo-capping 5′-RACE technique revealed that the genes encoding the “missing self” inhibitory receptors, Ly49A, C, G, and I, were transcribed from multiple broad regions in exon 1, in the intron1/exon2 region, and upstream of exon -1b. Ly49E was also transcribed in this manner, and uniquely showed a transcriptional shift from exon1 to exon 2 when NK cells were activated in vitro with IL2. Remarkably, a large proportion of Ly49E transcripts was then initiated from downstream of the translational start codon. By contrast, the genes encoding Ly49B and Q in myeloid cells, the activating Ly49D and H receptors in NK cells, and Ly49F in activated T cells, were predominantly transcribed from a conserved site in a pyrimidine-rich region upstream of exon 1. An ~200 bp fragment from upstream of the Ly49B start site displayed tissue-specific promoter activity in dendritic cell lines, but the corresponding upstream fragments from all other Ly49 genes lacked detectable tissue-specific promoter activity. In particular, none displayed any significant activity in a newly developed adult NK cell line that expressed multiple Ly49 receptors. Similarly, no promoter activity could be found in fragments upstream of intron1/exon2. Collectively, these findings reveal a previously unrecognized relationship between the pattern of transcription and the expression/function of Ly49 receptors, and indicate that transcription of the Ly49 genes expressed in lymphoid cells is achieved in a manner that does not require classical upstream promoters.
PublisherPublic Library of Science
URLhttp://dx.doi.org/10.1371/journal.pone.0018475
DOI10.1371/journal.pone.0018475
PubMed id21483805
NotesArticle no. e18475 is 14 pp.
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