In their recent report (PI and cosmid clones define the organization of 280 kb of the mouse H-2 complex containing the Cps-1 and Hsp70 loci. Immunogenetics 39:48-55, 1994) Gasser and co-workers erred when they stated that when the two 1-1-2 congenic strains B10.A(2R) and B10.A(1R)"were fed a minimal laboratory chow with no added vitamin A there was no significant difference between them in their susceptibility to glucocorticoid-induced cleft palate (Tyan, personal communication)." Published data clearly indicate that B 10.A(2R) like B 10.A is highly sensitive to glucocorticoidinduced CP when fed a 'minimal laboratory chow' such as Purina 5001 . However, B10.A(1R), which like B10.A(2R) is an H-2 recombinant strain between C57BL/10SgSn (inbred partner) and A/WySn and has the distal recombination site in the C4 : B 144 interval (see Table for H-2 haplotypes), has been reported to be as resistant to corticosteroid-induced CP as are C57BL/10 and B10.A(18R) mice (Tyan and Tyan 1993).
In addition, Gasser and co-workers (1994) suggested "that the H-2 a haplotype of B10.A is not a simple recombinant between H-2 k and the H-2 d haplotype of B10.D2, but that B10.D2 has a Cps-1 allele different from B10.A." I assume this point was made to explain why the H-2 d alleles in the Hsp70: BAT6 interval ofB 10.D2 confer resistance to CP and those of B10.A confer sensitivity. One explanation is that indeed B10.D2 and B10.A do have different Cps-1 alleles, derived from DBA/2 and A/WySn, respectively. However, if one assumes that Cps-1 is sufficient in itseff to determine sensitivity to corticosteroid-induced CP as appears to be the case here, it is difficult to explain the difference in sensitivity between B 10.A (sensitive) and B 10.A [(5R) (resistant: Gas-