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.
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