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Additive [d] and additive A- dominant epistasis [j] gene effects were found for fertile tillers in 10 dS m-1 of NaCl salinity.
A- dominant epistasis [l] gene effects were found for grains per spike in non-saline condition.
[d] dominant [h] additive A- additive epistasis [i] and dominant A- dominant epistasis [l] gene effects controlled K+ in non-saline and K+/Na+ ratio in low salinity.
Additive [d] additive A- additive epistasis [i] additive A- dominant epistasis [j] and dominant A- dominant epistasis [l] gene effects controlled grain yield in 10 dS m-1 NaCl.
Analysis of additional [F.sub.3] seeds from some of the heterogeneous lines suggested that low phytate may be controlled by recessive alleles at two independent loci that exhibit duplicate dominant epistasis.
The segregation indicated that low phytate was controlled by recessive alleles at two independent loci exhibiting duplicate dominant epistasis.
The duplicate dominant epistasis exhibited by the alleles at the two loci makes it necessary for both recessive alleles to be homozygous before an individual can express the low-phytate trait.
This is analogous to classical dominant epistasis that produces a 12:3:1 ratio of phenotypes in the [F.sub.2] of a dihybrid cross.
This ratio would suggest that two dominant genes control resistance, with dominant epistasis of RWA resistant alleles at one locus masking expression of alleles at the second locus.
This model hypothesized dominant epistasis with E1 epistatic to e7.
Option 1 is the single gene inheritance of photoperiod sensitivity, and Option 2 is the two gene model with complementary dominant epistasis.
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