Corn, like most plants, have two basic types of disease resistance systems. Quantitative, also called horizontal, resistance limits the spread of the pathogen by limiting the number and size of lesions. Qualitative resistance, also called vertical resistance, drastically limits the pathogen, often with sacrifice of the infected cells.
Quantitative resistance is initiated by detection of a general feature of the invading pathogen, such as the chitin component of a fungus like Exserohilum turcicum (cause of northern corn leaf blight). Chemical detection of the pathogen triggers production somewhat general antimicrobial enzymes in the area close to the invasion, limiting the pathogen. Quick detection and response results in fewer and smaller lesions. Relative differences for this resistance can be evaluated when varieties are compared when placed under the same pathogen pressure. This evaluation is usually done on a numerical scale ranging from very susceptible to very resistant. These ratings are always dependent upon equal exposure to the pathogen. Because reactions by the plant are metabolic processes that tend to decrease as the corn plant approaches completion of grain fill, relative maturity can be a factor in evaluating accurately comparing genotypes. Quantitative resistance ratings are not absolute but carry some relativity to disease pressure.
Quantitative resistance is usually affected by several genes in the host plant. This allows stability against races of the pathogen but also becomes somewhat awkward for the corn breeder to use in the breeding process because of the necessity of constant disease pressure.
Qualitative breeding is more attractive because it usually involves a single gene and it is more absolute- present or not. This gene produces a protein that responds to a specific protein in the pathogen, triggering a quick host cell that is different than that of quantitative resistance. For example, the Ht1 gene in corn, initiate stops the fungus (E. turcicum) from producing spores and further damaging the leaf. This single gene was attractive to breeders because of the ease of selection and strong control of the pathogen. Unfortunately, like in most cases of qualitative resistance, the single gene for resistance is matched with a variant of the fungus that no longer produces that specific protein detected by the host gene. Ht1 gene was used in much of the commercial corn hybrids during the 70’s but is of limited value now because of the increased frequency of the ‘race’ or pathotype not detected by Ht1 product. This is a common experience with other diseases as well and represents the plant breeder’s conundrum of balancing the expediency of breeding for qualitative resistance versus the probable short life of effective resistance.
The battle of corn genetic variability and pathogen genetic variability continues.
One of the more damaging virus diseases is caused by the combination of maize chlorotic mottle virus (MCMV) and any of the potyviruses maize dwarf mosaic virus (MDMV), wheat streak mosaic virus (WSMV) or sugarcane mosaic virus (SCMV). First identified in Peru in 1972, in Kansas and Nebraska in 1982 and Argentina in 1983. It was reported in China in 2010 and Kenya in 2011.
MCMV is transmitted by beetles, mainly Diabrotica species, and thrips (genus Frankliniella). These vectors also feed on possible alternate grass hosts of this virus. The virus can be transmitted by the larvae of Diabrotica in the soil or adult root worm beetles. MDMV RNA codes for the protein coat plus a few other proteins needed for replication but, like other plant viruses utilizes the host cytoplasm for materials and organelles to do the replication. Unless infected before V4 stage, the plants will not show stunting or early death but will have chlorotic mottling in leaves. Later plant feeding by adult beetles results in early death of ear husk leaves and small ears. In the USA, most severe damage because of early infection comes with continuous corn cropping and rootworm larvae. This is usually (always?) includes infection by one of the other viruses that are transmitted by aphids (MDMV and SCMV) or wheat leaf curl mite (WSMV). There is evidence of symptomless plants infected by MCMV if none of the other viruses are present. It is possible that this virus has been present on maize and other related grasses worldwide but has only became noted when the combinations with the other viruses caused significant symptoms.
Severe damage does require the complex interacting biology of the vectors, other virus hosts and corn growth stage. It needs to increase to a level that it can be noted in the field as well. Susceptible genotypes appear to be much more frequent than resistant but, in each case of a new occurrence, a few years of searching successfully identified resistance genotypes. This is consistent with our experience with several other known viruses infecting corn. An apparently new occurrence, then an investigation of pathogens, followed by a survey of genotypes for resistance and an investigation for the dynamics of disease. Eventually humans figure it out. All is well until the next disease outbreak. We should be thankful that the basic biology of that open pollinated species selected by humans was exposed to many environments resulting in large genetic variability.
Maize Dwarf Mosaic Virus (MDMV) is classified as closely related to sugarcane mosaic virus. It is vectored by aphid and infects some grasses other than corn such as sorghum and Johnson grass (sorghum halepense). Like other viruses it is constructed with a protein cover surrounding a nucleic acid, in this case being a RNA particle. It codes for 5 or 6 proteins including the protein cover. At least 5 genetic strains of the virus have been identified.
Severe symptoms in the field is linked to vectors and other host species being present while the corn plants are young (less than V4 stage), although older leaves can be infected. The virus is less likely to be transported within the plant and thus the plant may appear symptomless.
Resistance is linked to inhibition the virus being transported within the plant although the virus has been shown to replicate within cells where initially inoculated.
Although the virus may be damaging in susceptible varieties if the timing of infection is early, the damage is increased when other viruses are involved. The damage to susceptible hybrids in Southern corn belt of USA is greatest when the infected by MDMV and Maize Chlorotic Dwarf Virus (MCDV). The latter is vectored by leafhoppers such as Graminella nigrifrons. This virus also infects Johnson Grass, allowing this alternate host to be an overwintering host which is also a source of food for aphids and leafhoppers. The perfect storm is infected, perennial Johnson Grass, aphids and leafhoppers and late planted, susceptible corn. Effective control comes with effecting with these three factors.
The MDM virus moves with the endoplasmic reticulum in the corn cell’s cytoplasm to infect the chloroplasts. The chloroplasts appear to be the main site of virus replication. This must account for the major symptoms of initial yellow spots and the later mosaic appearance in leaves of susceptible varieties as the virus infects the parenchyma cells surrounding the vascular bundles.
Major virus replication occurring in chloroplasts and the fact that chloroplasts and their genetics originate in the female parent of a hybrid suggests that a source of strong resistance could come from the female parent. On the other hand, the spread of the virus within the plant could be related to other plant structures, possibly inherited by both parents.
MDMV, and its related potyviruses appear to be worldwide with potential hosts and vectors. Changing environments affecting vectors and alternate hosts affect the potential threat of these viruses.
Mollicutes are simplified bacteria having no cell walls and few organelles, but viruses are simpler as they are composed only of the genetic material of nucleic acid coding for its protein coat. Not having organelles causes many biologists to refer to them as ‘particles’ instead of living organisms. The nucleic acid center of the particle may be DNA or RNA, both coding for production of the protein coat. Not having the other cellular components such as ribosomes for protein synthesis, nor a supply of amino acids or energy source, viruses are completely dependent upon being parasitic of living cells. The nucleic acid component links into the host cells protein synthesis system to reproduce the virus particle.
Most plant viruses also infect insect species that feed on plants. Aphids, leafhoppers, beetles and mites are common vectors of corn viruses. Some are easily moved into leaf tissue by humans rubbing diseased tissue on non-diseased leaves. Many virus particles are able to move cell to cell through cell wall holes (plasmadesmata). Corn viruses commonly become most damaging after they reach the growing point, from which they infect the new cells. Most reach the growing point through the phloem.
Symptoms usually show as a mosaic chlorosis on leaves and dwarfness of the plants, but a few have darker green plants (maize rough dwarf disease). Some virus diseases are most severe when plants are infected with two viruses. Corn Lethal Necrosis severity is linked to Maize chlorotic mottle virus plus maize dwarf mosaic virus or wheat streak mosaic virus.
Resistance, either complete or partial, has been identified in corn to all known viruses. In some cases, it has required considerable effort to identify resistance sources when a disease is new to an area but the diversity in corn germplasm has always succeeded. For example, corn lethal necrosis suddenly showed up in Kansas but within a few years it was found that some older USA public inbreds were resistant. Likewise, it took only a few years for resistance to be found to this disease when it popped up in East Africa. The mechanism of resistance is not always clear but probably includes inhibiting the spread of the virus to the growing point. There is evidence that it could involve detection of the virus protein, turning on production of the resistance mechanism. It also could involve interfering with the translation of the virus nucleic acid code, resulting in inability to replicate the coat protein of the virus. This type of reaction is involved in some viruses that infect bacteria (these viruses are called bacteriophages). In this case the bacteria change the virus DNA or RNA code by making a simple nucleic acid switch, destroying the nature of the virus protein. This is the basis of the CRISPR technology now being proposed as a method of changing genes in higher plants.
Corn virus disease distribution and occurrence is greatly affected by environments affecting vector insects, alternative hosts and corn development. Another example of new challenges is inevitable, but the genetic diversity of corn will ultimately overcome the threat.
Spiroplasmas and phytoplasmas are single celled organisms grouped as Mollicutes and classified as bacteria but lack cell walls and much of the cytoplasm common to other bacteria cells. Most infect insects in which they multiply by using their own DNA to cause the host to produce the replication of the organism. The spiroplasma species, Spiroplasma kunkelii, causes the disease corn stunt, found in semi-tropical and tropical areas.
This species infects a few leaf hopper species (Dalbulus maidis, Dalbulus elimatus and Graminella nigrifrons), existing all year in the warmer climates. The spiroplasma replicates in the gut and saliva of these insects and consequently is injected into the corn plant upon feeding by the insects. From there the organism becomes concentrated on the phloem tissue, perhaps aided its own mobility. Ultimately, they must move to the growing point affecting cell elongation and thus stunting of the plant. The net effect, especially if the plant is infected while young, is yellowing of leaf tissue, stunting of the plant and eventual reddening of the leaf tissue perhaps as a result of anthocyanin accumulation because of no translocation to grain. This also can result in multi-branching in affected plants.
There are indications that occurrence of corn stunt in temperate zones is mostly related to the ability of the insects to withstand winter weather and thus related to winter temperatures as reported in an Argentine study (Journal of Economic Entomology, Volume 106, Issue 4, 1 August 2013, Pages 1574–1581). It is likely that the vectors are moved by winds from warmer areas during summers but infection into corn plants by midsummer does not allow sufficient movement to the growing point to cause meaningful symptom development. Late planted sweet corn has some vulnerability to this disease if conditions are right.
Another Mullicute causing a corn disease is a phytoplasma. This disease is called maize bushy stunt. It is found in Southern USA, Mexico, Central and South America. Although the organism differs from the cause of corn stunt, it is vectored by the same insects and causes similar symptoms. Both organisms may even be found in the same stunted plants.
Extreme small size of the organisms, complicated relationship with vectors, overlapping symptoms and interactions with host plant biology has resulted in limited information about nature of resistance. They deserve increasing attention in temperate zones if warmer winters allow expanding distribution of the vectors.
A corn disease only known to be in Africa since first discovered in 1949 was found in Nebraska in 2016 but by 2017 scattered fields in several USA Midwestern states. It was found in Argentina in 2017. The bacterium, currently named Xanthomonas vasicola pv. vasculorum (previously Xanthomonas campestris pv. zeae) can exist in dead infected leaves not only of corn but perhaps several other grasses. It is believed to spread to corn leaves in infected debris at least as young as V4 stage, probably during storms. From there, bacteria apparently enter to leaf through stomata. The bacteria move between cells reaching the parenchyma cells surrounding xylem cells of the smaller leaf veins. Receiving nutrition from the parenchyma cells and then multiplication in the xylem tubes, plugging these tissues results in dead, elongated streaks in the leaf tissues. These lesions tend to be limited laterally by large leaf veins and the plant resistance system eventually limits the length of the streak as well. It is probable that varieties differ in how quickly and completely the resistance system inhibits the expansion of the pathogen but it appears to not be significantly affecting grain yields on most hybrids. More study will better identify differences in resistance.
This disease seems to be only the most recent example of unpredictable occurrence of a corn pathogen. Did it arrive from South Africa or was it a mutated form of a bacterium that was already present on native grasses in the USA, adapting to vulnerable host genetics inadvertently bred into some corn hybrids? The wide and seemingly sudden wide distribution could possibly be explained by carrying with seed or even with ‘dust’ within grain. Wind, vehicles, ships, and people could move infected leaf debris. Proving that seed is the primary source is difficult because of the problem of adequately sampling.
A few other bacterial pathogens of corn such as cause of chocolate spot of corn (Pseudomonas syringae pv coronafaciens) and Goss Wilt appeared unexpectedly and fungal races such as race t of Biploaris maydis, race 1 of Bipolaris carbonum as well as several races of Exserohilum turcicum suddenly were found. We should expect this phenomenon to continue.
Apparent sudden 1969 appearance of this ‘new’ bacterial disease in Nebraska was a surprise. After initial observation, it was clearly severely damaging to only a few related hybrids, especially featuring the female parent A632, a widely used component of hybrids in the northern USA corn belt. It was also most frequent on continuous, minimum-tilled fields that had hail damage. Switching to more resistant hybrids and adjusting agronomic practices in the most affected fields, reduced the severe incidence of this disease for 30-40 years when again it appeared to be damaging in scattered fields from Indiana to Colorado. Where did it come from initially and why did it appear again several years later?
Surely it was occurring unnoticed, probably in both cases, before getting attention. This illustrates the difficulty of finding a new disease when the incidence is low. The pathogen, Clavibacter michiganensis var. nebraskensis, probably originated on other grasses such as green foxtail (Setaria viridis). Perhaps it was, and is, maintained on these grasses but some mutant allowed for pathogenesis on corn. The bacterial continue to exist in corn debris that can be carried by wind to corn leaves. With some exception, the bacteria mostly enter to the corn leaf through wounds, such as from hail and it is likely that natural infection generally occurs during heavy storms. If the infection occurs in 3-5-leaf plants of a very susceptible genotype, the bacterial advance to completely wilt the plant. Later infection on susceptible genotypes or on more resistant hybrids will result in elongated lesions as the bacteria tend to plug the xylem tissue.
Resistance can involve several genes, probably including the usual genetics for detecting the invader, communicating to adjacent cells to turn on appropriate DNA to produce anti-bacterial substances to inhibit the duplication and spread of the bacteria. Susceptibility must involve a deficiency in this system such as the gene(s) involved in recognizing this pathogen. Such a weakness can be realized after the disease becomes frequent enough to link its damage to specific genotypes but it is difficult when occurrence is low. This probably is associated with the reoccurrence of damage to a few hybrids elsewhere in the corn belt several years later.
This history and genetic interaction suggest that similar problems will continue as corn hybrids, cultural practices and potential pathogens forever change.
Stewarts wilt and leaf blight is caused by the bacteria species Pantoea stewartii (= Erwinia stewartii). This bacterium can only enter the corn plant through injury almost always associated with feeding by corn flea beetle. The beetle picks up the bacterium while feeding on infected leaf tissue of corn or other susceptible grass species. The bacteria can remain in the insect’s intestine for long periods, including between seasons.
Once injected in a corn leaf, the bacteria produce specific enzymes that attack cellular endoplasmic membranes. This results in leakage from the cytoplasm of affected cells, providing nutrition for increasing the number of bacteria within the tissue. If not stopped by the host cells, the bacteria plug the xylem tissue, causing a wilt of a young susceptible plant or elongated wilted lesion in more mature plants.
Plant defense system similar to other resistance methods, initially involves chemically detecting the presence of the intruder. After this detection, salicylic acid is produced causing the production and release of enzymes that effectively destroy the bacteria’s enzymes. This dynamic interaction, all controlled by genetics of the pathogen and of the host, affects the speed of cell destruction and the effect on the host plant.
Extreme susceptibility is most common in sweet corn varieties and few field corn inbreds. Resistance mostly involves several genes, probably affecting the detection of this bacterium and the speed of reaction, limiting the damage to a few cells.
Biology of the vector insect greatly affects distribution of Pantoea stewartii. Corn flea beetle (Chaetocnema pulicaria) overwintering success is affected by winter temperatures, surviving best in dry warmer temperatures. In the USA, these insects are favored in the mid-southern states. Sweet corn vulnerability to this disease increases with late planting because of the increase of the insect. Populations of this insect has decreased in recent years because of the increased use of a systemic insecticide seed treatment on corn. Consequently, the disease has also reduced.
Stewarts wilt biology includes that of host, bacterium and the vector insect.
Bacterial pathogenesis of corn differs from fungal pathogenesis mostly because of biological differences in the two types of organisms. Bacteria are single-celled organisms with a single chromosome without a nucleus in its cytoplasm. Cell division in bacteria results in a new, distinct individual cell, whereas fungal cells divide to form a filament, frequently maintaining cell to cell communication and specialization. Bacteria cell single chromosome simply replicates, then separates as a cell wall divides the cell into two halves, each with its own single chromosome. Fungal chromosomes are enclosed in a nuclear membrane, divide by mitosis during cell division but also can undergo meiosis forming single strands of the chromosome and thus exist as haploids until the nuclei fuse to form diploids. These structural and functional differences between bacteria and fungi results in different ‘strategies’ concerning adaptations of these organisms to changing environments. Mutations occur in both, but those in the single bacterium chromosome immediately results in a changed new individual bacterium. Mutation in fungal DNA may not take effect until recombination to form the homozygous recessive. Bacterial biology allowing rapid reproduction of the new forms allows adjustment to new hosts.
Bacteria are ubiquitous, distributed by wind, water, insects and animals. Rapid cell reproduction allows quick spread when in a nutritional environment. Despite their widespread presence, most species cannot infect living corn leaves. Leaves have evolved epidermal cells tightly held together and with a waxy covering, repelling water and prohibiting bacterial infection. Pathogenic fungi establish a multicellular mat (appresorium) from which it produces a penetration peg that enzymatically drills through the wax and epidermal walls to enter the leaf. Bacteria cells can enter through open stomata-some even have flagella to help swim to the stomata. Plant resistance systems can produce antibacterial fumigants to inhibit the bacteria from replicating and there is some evidence stomata close when faced with bacteria invasion.
Small size and few visible structural features has made it difficult to identify a bacterium causing a plant disease. Although some disease symptoms do become associated with specific species, confirmation usually requires culturing and chemical tests.
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.