GENETICS OF PLACENTOPHAGIA
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A single-locus explanation was rejected on the basis of the incidence of
ρlacentoρhagia in the progenitor strains and the high incidence of ρlacento-
phagia in the backcross generation and in the CXBG Ri-strain. Models
consiting of as few as two loci can be invoked. If two loci with average
dominance for placentophagia is the case, the alleles of the loci in question
are apparently not Isodirectionally distributed, in that the BALB∕cBy pro-
genitor does not possess all the alleles required to produce placentophagia in
100% of the females. Perhaps both progenitor genotypes harbor “increasors.”
For some reason, possibly epistasis, the BALB∕cBy progenitor genotype (A∕A,
+/+) results in placentophagia in 25% of the females, the C57BL∕6By
progenitor genotype (+/+, B∕B) results in placentophagia in 0% of the females.
The F1 hybrid genotype (A/+, B/+) also results in the promotion of
placentophagia in 0% of the females. The one-fourth of the B6CF1 × BALB∕c
backcross generation comprising the BALB∕c progenitor genotype, and the
one-fourth of the backcross generation comprising the double-heterozygous
genotype (F1) together can only account for the promotion of placentophagia
in 6.25% of the females of the backcross generation. The remaining two
genotypes of the backcross generation (A/+, +/+ and A∕A, B/+) must together
promote placentophagia in about 66.6% of the backcross females of those
genotypes. The high incidence of placentophagia in the first backcross and in
the (CXBH × CXBG) × CXBG Ri-strain backcross (62.9%) can be con-
sidered as further evidence of the presence of hidden increasors. Pursuing the
notion of hidden increasors further, we might consider that the two recom-
binant genotypes constituting 50% of the B6CF1 × BALB∕c backcross gener-
ation (A/+, +/+ and A∕A, B/+) promote placentophagia to a different extent.
The addition of one B allele to the BALB∕c genotype, or the removal of one
A allele from the BALB∕c genotype could conceivably produce incidences of
placentophagia of approximately 50% and 75%. The resulting incidence of
placentophagia in the entire backcross population would then be predicted to
be 0% of ¼ + 25% of ¼ + 50% of ¼ + 75% of ¼, or 37.5%. The observed value
for placentophagia in the backcross generation was 39.6% (19/48). The
expected value of 37.5% and the observed value of 39.6% are not significantly
different and in fact, in a sample of 48 mice represents a difference of only
one mouse.
The recombinant-inbred strains provided little decisive information be-
yond that obtained from the progenitor strains, F1 hybrid and backcross
generations, owing to our inability to match strain distribution patterns. The
incidence of placentophagia in the CXBG Ri-strain (43.75%) indicates that a
genotype producing approximately 50% placentophagia, such as that hypothe-
sized to exist in the backcross generation, is a distinct possibility. But neither
that observation, nor the incidence of placentophagia in the