Common rust of corn

​Puccinia sorghi causes common rust to corn. It is a biotrophic fungus, only infecting and receiving nutrition from living cells. This fungus has a complicated life cycle like most rust fungi. Spores carried by wind to the surface of the corn leaves, germinate and produce a gelatinous coating that allows it to stick to the corn epidermis. The hyphae produce an appresorium above a stomate, from which it enters to leaf.  The hyphae then penetrate adjacent cells, absorbing nutrition while keeping the host cells alive. Within 7 days, the fungus produces new spores (urediniospores), from the pustule formed from the erupted epidermis.  These spores then are spread to more corn leaf tissue. As the host plant matures towards the end of the season, the fungus produces teliospores with diploid nuclei as the two nuclei in the former hyphae are joined.  Teliospores will germinate, undergo meiosis and form haploid basidiospores that cannot infect corn. Instead, the basidiospores germinate to form hyphae that fuse with hyphae of a compatible mating type, forming hyphae cells with the two nuclei.  These hyphae infect only the alternate hosts of the genus Oxalis species occurring in the tropics.  These infections result in production of a different type of spore called aeciospores that will infect corn.  Pustules on those corn plants produce the urediniospores that will spread to more corn.  This complicated life cycle easily occurs in tropics but corn in the USA and other temperate zones is produced by continuous corn crops in semitropical areas such as Mexico and Caribbean Islands.  Spring storms from those areas carries the urediniospores north to infect young corn crops from which the pathogen is spread to other fields.
 
Corn plants express two types of resistance to this fungus.  Rapid collapse of the infected cell essentially deprives the fungus of nutrition.  As many as 24 variants of 4 different single gene loci have been identified with this type of resistance.  When effective, no rust pustules are formed. Unfortunately, in most cases, races of the fungus have been found that overcome each of these single gene resistance methods. 
 
More stability in resistance that allows a few pustules to form is inherited by 3-5 genes and is effected by a more common phenomenon of detection of the pathogen, inducing the promotion of chemicals that inhibit further spread of the fungus.  Multigene resistance shows the typical pattern of detection of the pathogen and production of anti-pathogen chemicals effective of killing and/or limiting the sporulation of the pathogen.  Some of this may be common to other corn disease reactions.  We have seen the interaction of this general resistance for P. sorghi and the northern leaf blight fungus Exserohilum turcicum.  If spring storms bring in rust spores immediately before we artificially inoculate plants with E. turcicum, we see fewer northern leaf blight lesions than expected. The opposite has also been found by others (Phytopathology 106:745-751) in which inoculating the plants with E. turcicum before applying P. sorghi spores resulted in a reduction of formation of rust pustules.  This is consistent with the view that some portion of the quantitative resistance system to these two pathogens is shared in corn plants.
 
As usual, single gene resistance is easier to detect and breed but the more long-term stability of adequate resistance to Puccinia sorghi comes with multigene, quantitative resistance.