The histocompatibility loss mutation H-2(dm6) was derived from a mouse treated with the chemical mutagen ethylnitrosourea, and previous mapping studies implicated D(d) as the affected locus. Southern blot analyses of DNA from H-2(dm6) cells did not detect major deletions in the D(dm6) gene, suggesting that H-2(dm6) was different from the previously characterized D region mutants H-2(dm1) and H-2(dm2). RNA blot analysis identified D(dm6) transcripts of appropriate size and a D(dm6) protein was immunoprecipitated from biosynthetically labeled H-2(dm6) cells. Interestingly, the D(dm6) protein showed no β2m association and was only precipitated by a mAb to the α3 domain. Furthermore, oligosaccharide maturation and low levels of surface expression of D(dm6) molecules were detected. However, the surface D(dm6) was nonfunctional as a target Ag in in vitro cytotoxicity assays, consistent with its original in vivo detection as a loss mutation. Sequence analyses of D(dm6) cDNA identified a single nucleotide base difference from wild-type, resulting in the substitution of a Trp to Arg at position 133. The significance of this substitution is discussed in the context of other class I expression variants.
|Original language||English (US)|
|Number of pages||6|
|Journal||Journal of Immunology|
|State||Published - 1991|
ASJC Scopus subject areas
- Immunology and Allergy