Several chemically mutagenized lines of soybean [Glycine mnu (L.) Merr
.] have shown enhanced nodulation and partial tolerance to high NO3- l
evels. Previous genetic analyses of hypernodulating or supernodulating
soybean mutants indicated that they were genetically controlled by re
cessive monogenes following simple Mendelian principles. In the presen
t study, we determined the genetic control of hypernodulating mutants
selected from two soybean cultivars, Williams and Enrei, and analyzed
the allelism of mutant genes controlling the hypernodulating phenotype
s. Reciprocal crosses between four hypernodulating mutants (NOD1-3, NO
D2-4, NOD4, and En6500) and two normally nodulated cultivars (Williams
82 and Harosoy 63) were made. The patterns of nodulation in F(1)s, F(
2)s, and F-2:3 progeny were visually evaluated at 14 d after planting
in the greenhouse. Chi squares for each progeny and homogeneity tests
for each cross were calculated. The results indicated that hypernodula
tion in the mutants studied was conditioned by single recessive genes.
Three mutants (NOD1-3, NOD4, and En6500) were controlled by a single
recessive allele rj(7), although they were isolated from distinctly di
fferent genetic materials. The allelism study indicated that another n
on-allelic mutant gene was identified which was responsible for hypern
odulation in mutant NOD2-4. This new gene has been tentatively designa
ted rj(8). With respect to genetic interaction between the two mutant
genes identified, the segregation ratio in the F-2 did not fit a class
ical pattern and therefore we speculated that these two genes interact
to modify expression in an unknown fashion. Hence, additional genetic
analysis is needed to clarify the genetic interaction between rj(7) a
nd the proposed rj(8) gene.