Southern rust of maize (agent, Puccinia polysora) is the cause of major crop losses throughout the tropics and subtropics. During the past three decades we have been breeding field and sweet maize for general resistance in Hawaii, and assessing the nature of genetic control. The disease spreads only by uredospores, and infection optimizes during our wet winter months. Several hundred inbreds were initially evaluated under rust epiphytotics in Hawaii, Nigeria, Mexico, Philippines and Colombia. Multiple races of the pathogen appeared to occur at these locations, since racially specific resistance based on the Rpp9 allele on Chromosome 10 was ineffective. General resistance proved to be rare in temperate germplasm and virtually nonexistent in temperate sweet corns. Inheritance of durable, general resistance was then studied in a series of RILs, GMAs and diallels. Resistance characterized about 20% of tested tropical inbreds and was observed to be a mature-plant trait (described as a “slow-rusting response”). A stable intermediate tolerance characterized about 20% of tested inbreds. Hybrids were intermediate to parents. Two sets of RILs from crosses of susceptible and intermediate inbreds could be interpreted on a single-locus basis. RFLPs illuminated a major QTL on Chromosome 6 from Thai inbred Ki14. Tropical sweet corns bred for intermediate resistance appeared also to have a single major gene, with some evidence that it is linked to shrunken-2 locus on Chromosome 3. GMAs from crosses of highly resistant lines with susceptible lines could be interpreted as digenic. Synthetic MIRSYN3 was based on 19 highly resistant inbreds and showed a stable resistance through 6 cycles of recurrent selection. Resistances to polysora and common rusts (P. sorghi) were not correlated (R²=.004). The conversion of inbreds to high general resistance has been successful enough to suggest oligogenic control, with perhaps two major QTL loci on the two historic maize genomes.