The relationship between theH-2 loss mutations ofH-2^da andH-2^db in the mouse

Abstract

The mouse strain B10.D2-H-2^da carries the mutantH-2^da allele, derived after chemical induction, and this has been shown to be a gain and loss mutation involving theH-2D^d locus.BALB/c- H-2^db, derived spontaneously, is a loss mutation only, and appears not to involve theH-2D^d, but rather theH-2L^d locus. The two mutations effectboth graft rejection and serologically detected H-2 specificities (Type II mutation). In the experiments described in this study, theloss mutations in theH-2^da andH-2^db mutants have been compared by skin grafting, and by direct and absorption serological techniques: (1) By skin grafting, using the well established complementation method, it has been shown thatH-2^da andH-2^db do not complement each other, i.e., the mutation in both occurred at the same ‘locus.’ However, by appropriate selection of donor and recipient, it has become clear thatH-2^da had a greater loss than didH-2^db, althoughH-2^da includes the loss found inH-2^db. (2) Serological studies have demonstrated that H-2D.4 was altered inH-2^da, but not inH-2^db; ‘H-2.28’ (detected by D-28b and D-29) was decreased or lost in both mutants;H-2^db anti-BALB/c failed to react withH-2^da; both mutants reacted similarly with D-28 sera. In addition, sera made usingH-2^da as donor did not contain an anti-H 2.28 antibody. The loss mutation involvingH-2^da therefore appears to have led also to the loss of H-2.28 as found inH-2^db. We conclude that theH-2^da strain arose after a complex mutation or recombination event which involvedboth theH-2D^d locus and the closely linkedH-2L^d locus, whereasH-2^db affects only theH-2L locus.