Pea (Pisum sativum) dominant for the fundamental color gene A showed a high level of resistance to Globisporangium ultimum (formerly Pythium ultimum) seed rot. Reciprocal crosses demonstrated that, with our materials, such resistance was associated with the testa (seedcoat) phenotype but not the embryo phenotype. Dominance of A over a was complete for this trait. Neither wrinkled seed form (r) nor green cotyledons (i) diminished resistance when A was dominant, although both recessive alleles diminished resistance when seeds were borne on white-flowering (a) plants. The product of the A gene functions in the pathway leading to flavonoids, including proanthocyanidins (PAs) and anthocyanidins. We found that resistance to G. ultimum seed rot was closely associated with not only dominant A but also testa PAs and testa sclerenchyma. Even A testas that lacked anthocyanins but contained PAs and sclerenchyma showed a high level of seed rot resistance. Moreover, a mutation removing PAs and sclerenchyma in a narrow zone from the hilum to the radicle markedly increased susceptibility. The PAs in pea testas were predominantly prodelphinidins in seeds from purple-flowered plants (A B) and procyanidins from pink-flowered plants (A b). Compared with procyanidins, prodelphinidins have higher antioxidant activity but are more likely to sequester iron, a particular concern with dry pea. Although A B testas were more resistant than A b to seed rot, the difference seemed too slight to militate against growing pink-flowered pea. We stressed the need for more histological comparisons of A B and A b testas, and we indicated that genes and their phenotypic effects examined during the current study could be useful for modeling biosynthesis of PAs and related cell walls.
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