Tandem repeats modify the structure of the canine CD1D gene. (19th September 2012)

• Record Type: Journal Article
• Authors: Looringh van Beeck, F. A.; Leegwater, P. A. J.; Herrmann, T.; Broere, F.; Rutten, V. P. M. G.; Willemse, T.; Van, I.
• Is Part Of: Animal genetics. Volume 44:Number 3(2013:Jun.)
• Page Start: 352
• Page End: 355
• Publication Date: 2012-09-19
• Subjects: Animal genetics -- Periodicals; 572.8
• DOI: 10.1111/age.12002
• Languages: English
• ISSNs: 0268-9146

Abstract

<abstract abstract-type="main" id="age12002-abs-0001"> <title>Summary</title> <p>Among the CD1 proteins that present lipid antigens to T cells, CD1d is the only one that stimulates a population of T cells with an invariant T‐cell receptor known as NKT cells. Sequencing of a 722 nucleotide gap in the dog (<italic>Canis lupus familiaris</italic>) genome revealed that the canine <italic>CD1D</italic> gene lacks a sequence homologous to exon 2 of human <italic>CD1D</italic>, coding for the start codon and signal peptide. Also, the canine <italic>CD1D</italic> gene contains three different short tandem repeats that disrupt the expected gene structure. Because canine <italic>CD1D </italic>cDNA lacks sequences homologous to human exon 2 and 3, the functionality of canine CD1d protein may be affected, and this could have consequences for the development and activation of canine NKT cells.</p> </abstract>