All corn pathogens and their host have interacting biology. The rust fungi take the interactions to a higher level. Being obligate (biotrophic) parasites, these fungi can only obtain nutrition through living cells, requiring rust fungi to keep the corn cells alive long enough to absorb photosynthates for reproduction and spreading to more living cells in the same host species and then to finally infect an alternative species to complete its sexual cycle.
The common rust species, Puccinia sorghi, spreads to the most temperate zone corn areas from areas with year around corn, such as tropical area. The means of distribution are urediniospores produced on infected, living corn plants. Easily lifted to high altitude winds, especially with storms moving northward in the USA the spores are deposited in the whorls of young corn plants. Requiring only 6 hours of moisture, the germinating spores infect through the stomata of newly emerging leaves. From there hyphae produce an haustoriium that penetrates the cell wall but not the cell membrane, allowing the corn cell to continue with photosynthesis. Instead of the resulting photosynthates moving elsewhere in the plant, it is absorbed by the rust fungus. The time from infection to pustule formation varies with the host genetics but it is only a matter of days before the fungus produces the red urediniospores and spread to other areas on the same plant and elsewhere in the area. Multiple infections of a corn plant, can draw sufficient photosynthates to the fungus to cause light grain weight and total grain loss.
Urediniospores of Puccinia sorghi only infect corn. As the pustule ages, perhaps because the host cells die, the fungus produces black spores (teliospores) that can only infect Oxalis (shamrock) species of plants. After infecting the Oxalis plant, the fungus undergoes sexual reproduction and eventually produces another spore type (aeciospores) that can infect corn. However, with Oxalis plants not living through the winter in most temperate area, this part of the fungus life cycle is only completed in tropic and semi-tropic regions. It is there that maximum genetic variability in the fungus occurs. Also in those areas, the cycle is completed with production of new urediniospores that are carried by winds to temperate areas. Consequently, corn infection in temperate areas is dependent upon movement of urediniospores from where corn is grown most of the year.
Resistance by the corn plant must either limit the successful penetration through the stomata and/or successful penetration of the cells. This results in few pustules on the leaves. This general or horizontal resistance is controlled by many genes and is considered stable against many races of this pathogen.
A more complete resistance resulting in no pustules starves the fungus by causing the host cell to collapse and therefore produce no nutrition for the rust fungus. No pustules develop if this gene is effective against the attack race of the fungus. This vertical resistance is controlled by a single gene. But, of course, as is common with single gene resistance systems, a race of the pathogen can overcome the resistance. Several single genes in corn have been identified and likewise several races of Puccinia sorghi have been identified that can overcome each of the resistance genes.
Natural selection for preferable genetics works for pathogens and their hosts!
Visit us at the ASTA in Chicago, Dec 9-12 (booth G207)
About Corn Journal
The purpose of this blog is to share perspectives of the biology of corn, its seed and diseases in a mix of technical and not so technical terms with all who are interested in this major crop. With more technical references to any of the topics easily available on the web with a search of key words, the blog will rarely cite references but will attempt to be accurate. Comments are welcome but will be screened before publishing. Comments and questions directed to the author by emails are encouraged.