Disease resistance is an extremely valuable control measure of rusts in cereal crops and is based, almost entirely, on simple procedures of identification and incorporation of major genes for resistance into economic varieties. Usually, several loci that carry these genes are known in each plant species. Frequently, several alleles at a locus can be distinguished on the basis of their reaction to various races of the pathogen. In spite of the vast array of resistance genes now known, their use has been sharply limited by the restricted number of loci in each species. The result has been a never-ending cycle of (1) releasing a variety resistant to prevalent races, (2) finding it susceptible to new races of the pathogen appearing a few years later, (3) breeding resistance to the new races, and (4) releasing the new variety only to find it susceptible, a few years later, to yet new races of the pathogen. Thus, breeding for rust resistance in cereals has been so repetitious that the value and use in disease control of genes that condition resistance to only a portion of the possible rust races is now widely questioned.' Although major genes for rust resistance have been used extensively, little is known about their fine structure. This is probably due to the fact that in crops, where resistance genes have been of maximum importance, genetic analyses requiring large test-cross progenies are not feasible. Economic and biological considerations, however, provide compelling reasons why studies on the structure of genes for rust resistance should be made. The system of genetic resistance to rust, Puccinia sorghi Schw., in maize, Zea mays L., is apparently parallel to that found in other cereal crops. In maize, there are at least five loci (Rpl, Rp3, Rp4, Rp5, and Rp6) at which dominant genes for rust resistance occur.2-6 Rp, is located in the short arm of chromosome 10 and was considered to occupy the terminal position on the genetic map.3'7 Recently, Rpi has been shown to be located between Rp5 and Rpe which are 1.1 and 2.1 map units, respectively, from it.' Orientation of these genes with respect to the centromere is not known. Rp3 and Rp4 are independent of Rpi. On the basis of genetic studies and disease reaction, 14 alleles, Rpia, Rp b... to

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Gene Ht2 that conditions a form of chlorotic‐lesion resistance to Helminthosporium turcicum Pass, was identified in the Australian dent corn (Zea mays L.) inbred NN14. Inbred NN14 also carries a second gene at the Ht locus. The two genes are not linked. Gene Ht2 conditions a lower level of resistance than does Ht but the two genes interact together to condition a higher level of resistance than either gene alone.

SummaryThe nature of gene action conditioning the quantitative type of resistance in maize (Zea mays L.) to Northern leaf blight caused by Helminthosporium turcicum Pass. was studied in crosses between four Australian resistant inbred lines (D21, HB, 21H, and 25) and three tester inbred lines (susceptibles H10 and 701, and moderately resistant Oh43). Populations composed of the P1, P2, F1, F2, BC1P1 and BC1P2 generations were studied for the 12 possible crosses in 1966 and with the addition of F3, BC1P1S and BC1P2S families for four crosses in 1967.Additive, dominance, and epistatic gene action were detected by analysis of generation means. Additive gene action was of major importance in all crosses in both years. The relative importance of non‐additive effects was generally small and varied with the population involved and, to a lesser extent, with the year of study. Although biased by limitations in experimental and analytical design, estimates of components of genetic variance were in general agreement with the results of the generation mean analysis.It was concluded that leaf blight resistance in these lines was conditioned by a relatively low number of genes, primarily additive in effect. Breeding for resistance to this disease should be effectively accomplished by such simple procedures as phenotypic recurrent selection or mass selection.