MENDELIAN INHERITANCE OF CERTAIN PATHOGENIC CHARACTERS OF PUCCINIA GRAMINIS TRITICI

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Abstract
Crossing and selfing studies with physiologic races of Puccinia graminis Tritici have shown that certain pathogenic characters are dominant to others. The "0" type of infection (absence of rust pustules) on the variety Kanred was found to be dominant to the "4" type (large rust pustules), so that when a race producing the "0" type was crossed with a race producing the "4" type the hybrid rust produced the "0" type. When the hybrid race was selfed, the "0" type occurred about three times as frequently in F2 as the "4" type, a fact indicating that rust behaviour on this variety is governed by a single-factor pair. The "4" type of infection on the variety Mindum normally was dominant to the "1" type (very small pustules) and occurred about three times as frequently in F2. The "1" type of infection on the emmer variety Vernal was dominant to the "4" type and recurred in some crosses, about 15 times as frequently in F2 as the "4" type. Rust behaviour on this variety appears to be governed by duplicate factors, each factor being capable of exerting the same effect. Evidence derived from a study of the F2 populations of two crosses between races 9 and 36 indicated that the factors governing rust behaviour on Kanred, Mindum, and Vernal, were different and were inherited independently of each other. In crosses in which the two parent races produced different infection types on the variety Marquis, the cytoplasm of the maternal parent race appeared to influence pathogenicity on this variety.As a result of these studies it is concluded that despite the binucleate condition of stem rust in its uredial phase, the genes function as if they were present in a single diploid nucleus, and that, owing to fusion of the nuclei in the teliospore and subsequent meiotic divisions, independent segregation of factors occurs as in higher plants. The crossing of physiologic races and the selling of the hybrids lead to various recombinations of existing pathogenic characters that may result in the formation of new physiologic races without involving the creation of pathogenic characters not possessed by the parent races.

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