Resistance to northern leaf blight fungus

​After penetration of the leaf epidermis by Exserohilum turcicum (Setosphaeria turcica), adjacent corn cell plasma membrane detects a common protein component of the fungus chitin wall structure.  In response, the cell produces products to inhibit or at least slow the growth of this fungus.  This basic defense method is common in plants as they ward off many potential pathogens.  The only microbes successfully spreading sufficiently to receive nutrition from the plant are those either avoiding detection or limiting the damage from the plants response. This is the definition of a pathogen.
 
Corn varieties vary in the quickness and strength of the response and E. turcicum isolates differ in quickness of growth as it heads towards the vascular tissue in the leaf tissue.  It appears that 3 or 4 corn genes are involved in effectively detecting and slowing down this fungus from reaching the vascular tissue.  It is probable that minor genes also influence the effectiveness of this resistance system.  This system of resistance effectively limits the number of lesions but can be overwhelmed if the pathogen numbers are intense.  Consequently, resistance ratings need to be expressed with some relativity to disease pressure and reactions of other varieties.
 
There are some single genes in corn that can more drastically limit the disease.  HtN1 is a gene that significantly delays development of lesions and, consequently, slowing the spread of the northern leaf blight in a field.  This gene was discovered and later isolated from an old Mexican variety.  Other single resistance genes named Ht1, Ht2 and Ht3 initially found in varieties of tropical corn, popcorn and Tripsacum.  Each of these single genes produce products that limit the fungus’ ability to produce spores but do not restrict the fungus from reaching the vascular tissue. These genes have been crossed into some corn varieties but the futility of use of these genes eventually becomes realized as the selection pressure within the fungal genome results in a ‘race’ of the fungus that is unaffected by the host gene. 
 
As with most corn diseases, resistance systems affected by multiple genes and limiting the success of the pathogen to establish lesions is the most stable.