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- Title
Further Evidence That LOCR Is an Rh System Antigen.
- Authors
Coghlan, G.; Zelinski, T.
- Abstract
Background: The low incidence rod cell antigen, LOCR (700.53), was the subject of a full-length report in 1994. In spite of the fact that LOCR(+) red cells display altered expression of c or e antigens, formal genetic evidence fell just short of that required to place LOCR in the Rh blood group system, largely because one of the families studied (8 children) was not informative for RH. The current study was undertaken in an attempt to resolve this issue. Study Design and Methods: Genomic DNA from family members segregating for LOCR was amplified by the polymerase chain reaction and analyzed for repeat polymorphisms using markers (D1S1612, D1S1597, D1S552 and D1S2134) that flank RH. Each family was subsequently analyzed to determine the linkage relationships between markers and to establish the inherited haplotypes. Results: Peak lods for linkage between LOCR and D1S552 for combined paternal and maternal meioses were 2.41, with no evidence of recombination (individual family counts of 7:0 and 3:0). Those for the LOCR:D1S1597 pair were 1.51 for maternal meioses, again with no evidence of recombination. Analysis of the inherited haplotypes from the members of the previously mentioned RH non-informative family revealed that all LOCR(+) children inherited the same set of chromosome 1 p markers from their mother, whereas the LOCR(-) children inherited her other copy of chromosome 1p. Conclusions: With consideration to the previously determined peak lods of 2.11 between LOCR and RH we undertook the current study in an attempt to assign LOCR to the Rh blood group system. Since there is no recombination between LOCR and the RH substitute marker D1S552 in the RH non-informative family (peak lods of 1.81), we suggest that LOCR is an Rh system antigen. This conclusion is strongly supported by haplotype analysis, as all LOCR(+) individuals display a haplotype that is not seen in their LOCR(-) siblings.
- Subjects
ANTIGENS; ERYTHROCYTES; RH factor; GENETIC polymorphisms
- Publication
Transfusion, 2001, Vol 41, p5S
- ISSN
0041-1132
- Publication type
Article