Identification of new occurrences of corn diseases in the USA rightfully gets attention of people growing corn. Since my introduction to corn pathology in 1971, I have witnessed to increased intensity of pathogen races for southern corn leaf blight, northern leaf blight, northern leaf spot, and common rust. We have seen increased widespread destruction of pathogens causing gray leaf spot, sudden occurrence of Goss Wilt that seemed temporarily controlled and the more recent reemergence in new areas. Head smut, once common in high plains of Texas suddenly showed up in areas of Minnesota and Canada. Eyespot, once known only in Japan, suddenly became common in Southeaster Minnesota and Wisconsin. Corn Lethal Necrosis caused by combination of Maize Chlorotic Mottle Virus and maize dwarf mosaic virus or wheat streak virus suddenly was found in Nebraska and Kansas, and more recently in central Africa. More recent attention has been drawn to outbreaks of bacterial leaf streak and tar spot.
Severe crop losses have been avoided after these diseases were acknowledged, resistance was identified, and cultural practices modified. Relatively quick identification of the disease, study of its dynamics, genetic diversity in maize, corn breeding efforts has allowed reasonable control of the new disease occurrences.
Genetic diversity works both ways, however, as breeders inadvertently select for other favorable traits, usually unaware that a new race of a pathogen, or environmental variable, exposes the newest corn hybrid to a disease. We usually only know of such a disease after it had increased in intensity sufficient to grab the attention of a grower or agronomists who has the diagnosis by a pathology specialist. How many years has that new race or pathogen been infecting a few plants in center of corn fields before it got attention? Bacterial leaf streak was identified in 2016 in 9 states. How long had it been present? After the problem of the race of fungus causing northern leaf blight that could overcome the Ht1 gene, it was reported in multiple locations across the Midwest USA.
Current corn growing practices should increase the probability that new pathogens are developing each season and noting strange lesions or other potential disease symptoms should be reported to specialists to set off further searches.
Elongation of the seedling radicle becomes the primary root, sustained by nutrition from the seed endosperm. Extension of hypocotyl towards light includes stem nodes as leaves are produced and eventually extended above the soil surface. Leaves thus produce the carbohydrates to fuel growth of roots from below ground nodes. These secondary roots initially extend laterally but geotropism takes over as the roots grow downwards. Environments and genetics affect the direction, volume and effectiveness of these roots in providing uptake of nutrients and water. These factors also affect the anchoring of the plants and ability to withstand strong winds. More lateral growth provides more strength against midseason lodging factors whereas deeper roots may provide better water uptake during drought periods.
Growth of roots is dependent upon a supply of carbohydrates moving from leaves to the root tips for production of new cells, for root cell growth, uptake of minerals into roots and the transport of minerals to the corn plant parts above the soil surface. Movement of glucose to the roots through the phloem is also an energy consuming process. Root growth competes with above-ground growth for carbohydrates. Distribution of this energy source is affected by genetics, especially those affecting hormone production by root tips.
Root volume tends to continue increasing until about two weeks after pollination. Carbohydrate translocation direction is affected by the hormones produced by kernel embryos, creating competition with the roots. Part of root cell function is a defense against the multiple soil organisms surrounding the roots. Reduction of carbohydrate supply begins to allow more saprophytic fungi to invade the root system. Increases in competition with developing kernels increases the deterioration of the root tissue. The next 40-50 days after pollination become critical to maintaining life in corn roots.
Much of the US Midwest was planted to corn much later than normal because of weather problems. Instead of corn planted in relatively cool soils and cooler air temperatures of April and May, corn was planted in June. Temperate zone adapted corn apical meristem is stimulated to switch from producing leaf and stalk cells to flowering structures by accumulation of heat energy estimated by growing degree heat units. June and July temperatures being warmer than the usual April and May temperatures should lead to a quicker change to the apical meristem switch to flowering structures.
Plant height is determined by the number of stalk cells produced by the apical meristem plus the elongation of the cells mostly affected by water infusion before the cell walls solidify. It will be interesting to see if the rapid growing degree accumulation of the extreme late planted corn reduce the number of stalk cells than normal, resulting is shorter hybrids than expected. Will all hybrids show the same reaction? Will we see a difference in timing between pollen production and silking? We should learn something new about corn maturity and heat during the next few months.
The blog post below from Corn Journal 10/5/2017 speaks to the issue of heat units and flowering.
RELATIVE CORN MATURITY
Heat is a major energy factor influencing the development of corn plants and the ultimate grain yield. Cellular respiration rates increase as temperatures go up. Photosynthesis rates also respond to increased heat as well. It seems reasonable to assume that practically every physiological function in the corn plant is affected by heat energy.
This includes the transformation of the apical meristem from producing leaf buds to production of the tassel. This happens in corn plants at about the V6 stage. Many, many years ago, I dissected young corn plants of hybrids of nearly all maturities sold by a major seed company looking for this change in the apical meristem. The change visible under a microscope, was nearly perfectly correlated with our final classification of the relative maturities of the hybrids. This is consistent with the view that the first influence of temperature on corn maturity occurs early in the season. It is probable that temperatures further affect further development of the differentiated apical cells into mature tassels. We attempt to express the daily temperatures that could affect the timing of pollination with averaging high and low daily temperatures but accurately depicting the duration of a high or a low temperature is difficult. We know that it does affect, but like much of growing crops, we know of the principles but not all the specifics.
Grain fill period seems mostly fixed to about 55 days but there are studies that show low night temperatures can extend the period to formation of the abscission layer, thus increasing grain yield (Elmore, R. 2010. Reduced 2010 Corn Yield Forecasts Reflect Warm Temperatures between Silking and Dent. Integrated Crop Management. Iowa State University, 9 Oct. 2010). It is likely that each hybrid differs in its reaction to temperature during this period.
Given the difficulty of accurately measuring the specifics of temperature interactions of corn plant morphological development, cellular function such as photosynthesis, respiration rates and translocation rate of sugars It is best that we simply compare hybrids for their usual time to harvest moisture. It is all relative.
Most people working with corn concentrate on the name of the disease while leaving the nomenclature of the pathogen up to specialists. It is confusing when one sees pathogen names change but the disease name remains the same. Name changes usually occur as taxonomists attempt to clarify the relationships among species of fungi. Further investigations often discern variants within a species especially affecting their pathogenicity.
Many corn leaf pathogenic fungi are part of a group of fungi called Ascomycetes. The sexual reproduction state of these fungi occurs after the fusion of individuals mating types, forming diploid nuclei which undergo miosis and produce haploid spores within a sac called an ascus. These spores germinate to produced hyphae that asexually reproduce by spores called conidia. The ascus stage is rarely found in nature because the prominent pathogenic stage is linked to the asexually produced spores. The formal ‘rule’ for fungal taxonomists is to name the fungus by the sexual name. Consequently, the formal name of the Northern leaf blight is Setosphaeria turcicabecause the sexual stage belongs to the genus Setosphaeria. However, the fungus was mostly known as Helminthosporium turcicumuntil more recent research distinguished it from others previously named Helminthosporium such as those causing southern corn leaf blight. Now the most widely used name is Exserohilum turcicumbecause of the shape of the asexual conidia. Compendium of Corn Diseases fourth edition lists the causal organism of northern leaf blight as “Setosphaeria turcica(syns. Bipolaris turcica, Drechslera turcica, Exserohilum turcicum, Helminthosporium turcicum and Trichometashaeria turcica). Only one fungus species but with different names.
Southern leaf blight fungus currently commonly named as Bipolaris maydis, has a similar nomenclature record. Compendium of Corn Diseases, fourth edition, lists the pathogen as Cochliobolus heterostrophus(syns: Bipolaris maydis, Drechslera maydis, Helminthosporium maydisand Ophiobolus heterostrophus). Again, one fungus but different names as sexual stage as recognized and relationships with other fungi is acknowledged.
Another aspect of pathogen names is distinction of variants that result in different pathogenesis. Some of these are probably simple genetic differences within a species and are often related to specific genes for resistance within corn varieties. Race 1 of E. turcicumovercomes the Ht1 gene for resistance in some corn varieties. Race T of B. maydisovercomes corn varieties with the T cytoplasm for male sterility. In some cases, the pathogen variant is described as a subspecies such as the bacteria causing Goss Wilt (Clavibacter michiganensissubsp. nebraskense). Bacterial leaf streak cause is Xanthomonas vasicola pv. vasculorum.
Taxonomists attempt to name pathogens according to the latest research. Pathologist attempt to use the most meaningful terminology to communicate information about the disease. Growers need to concentrate on the dynamics of the disease and try not to be confused with the pathogen names.
Humans are compelled to assign names to things, partly for the practicality to communication and partly to bring order to the life we witness. A system called binomial nomenclature was formalized by Carl Linnaeus in 1753 in which living organisms were named by genus and species. These Latin-based names were intended to assign individuals that were morphologically similar to the same genus but separate species if they were sufficiently distinct and did not sexually cross in nature. For most flowering plants, this naming system is clear. Sunflower species in genus Helianthusare morphologically distinct from corn in genus Zea. Most specialists (taxonomists) recognize 6 species of the genus Zea of which Zea mays (corn) and Zea diploperennis (teosinte) are most prominent.
This nomenclature often is dependent on assumption that distinct species do not intermate in nature and thus not produce intermediate types. Consequently, the emphasis in higher plants includes morphological features of the flowers. This principle was also applied to micro-organisms although the difficulty of recognizing morphological features often required microscopes.
Difficulty in identifying multiple distinct characters of fungi is further complicated by rarity of sexual reproduction. Many corn fungal pathogens reproduce asexually producing huge numbers of spores to spread to new host surfaces. Consequently, initial nomenclature for a fungal pathogen is based upon the features of these spores. The fungus causing southern corn leaf blight of corn was name Helminthosporium maydisbecause the asexual spores, called conidia, were long, darkly pigmented and slightly curved. This species was distinguished from Helminthosporium carbonum, cause of northern leaf spot, because the latter had similar, but slightly darker spores without curves. H. carbonumtended to infect corn in cooler areas than H. maydis but the presence of race T of H. maydisallowed massive mingling and sexual reproduction between two species resulting multiple intermediate conidia features and corn lesions.
Northern leaf blight of corn is also caused by a fungus with long dark conidia and thus was assigned to the genus Helminthosporium, called H. turcicum. It was later realized that a major difference in spore shape between other Helminthosporium species what a protrusion on the spore called the hilum and thus the genus name was changed to Exserohilum. H. maydisand H. carbonumshare a conidial feature of germinating at both ends and thus put in the genus Bipolaris. Current accepted names for these pathogens are Bipolaris maydis, Bipolaris zeicolaand Exserohilum turcicum.
We humans try to communicate a complex reality of living organisms with a simple nomenclature that is vulnerable to change as we learn more about these organisms.
This fungus more commonly known as Bipolaris zeicola is usually an insignificant corn pathogen that is a good example of the complexity of dynamics between corn and potential diseases. Both the host and fungus genetics interact within their environments. The fungus is saprophytic digesting and growing on dead plant tissue, especially in grasses. Some genetic variants of the fungus produce a toxin that kills a small area of a living leaf, forming a lesion, allowing the fungus to receive nutrition. The plant tissue responds by limiting the fungus from further growth. The fungus responds by producing spores, to spread to more potential host areas. This interaction is common throughout nature. Corn interaction is probably clearer because of the extreme genetic variability of the host across years and environments.
Race 0 of B. zeicolacauses very small flecks on most corn varieties. It apparently can be found on dead corn tissue, perhaps on dead tissue on living plants that were killed by other causes. Race 1 of this pathogen shows up periodically as a susceptible inbred is grown. It produces a toxin that kills leaf tissue in area of about 1 cm in length and 0.5 cm wide before the plant successfully stops the pathogen but spore production spreads it to more leaves. It also can invade the kernels on ears. Susceptibility must be genetically simple, as it appears occasionally in breeding programs. It can be significant to seed production. Race 2 became notable especially on a different set of inbreds, such as W64A especially in the northern USA corn belt. Those inbreds susceptible to Race 1 were not susceptible to Race 2 and vice-versa.
Race 3 became apparent after invasion of the US corn belt by Race t of a related species Helminthosporium maydis(Bipolaris maydis) in 1969-1970. The two species have been shown to cross in culture and it is hypothesized that the mix of the two species with the northern exposure to the other species allowed for new genetic combinations. Race 3 of causes longer more narrow lesions on susceptible inbreds. Race 4 of B. zeicola became apparent in 1980 in seed production fields with B73 derived inbreds. These lesions differed from Race 3 with wider lesions and significant losses in seed production fields that spraying is needed. There is evidence that this race, and probably others, successfully invades the production field by producing initial spores on nearby grasses.
Genetic variability in potential pathogens, multiple hosts and genetic variability in the corn species and among ‘new’ varieties can result in unexpected corn diseases. We usually don’t become aware of the new interactions until the incidences are large enough to get attention.
Exserohilum turcicum (Helminthosporium turcicum) has been known as a pathogen of corn probably as long as corn has been cultivated in the humid fields. This fungus overwinters in diseased leaves, produces spores that spread to new crop leaves that germinate and penetrate the leaf tissue. The mycelium grows in the leaf tissue, plugging the veins until the plant resistance system restricts the growth, causing the fungus to produce a lesion upon which the fungus produces spores and thus spreads further on the same plant and nearby plants. Time from infection to lesion formation is about 2 weeks, although the plant’s resistance response may affect this time frame.
Corn genetics is a major factor in preventing this fungus from reaching the vascular system within the leaf. Selection of genetics for reduced number of lesions is practiced by most corn breeding programs. This system allows the fungus to reproduce but at a slower and less successful rate than more susceptible genetics. Three or four genes are involved in this type of resistance. This type of resistance is called horizontal or multigenetic resistance.
Environments favorable to the fungus, such as diseased leaf tissue on surface of non-tilled field and frequent rain may increase initial spore production and thus more infection, resulting in increased lesions on even the more horizontally resistant hybrids.
A type of resistance that allowed the fungus to reach the leaf vein but prohibited normal lesion production with fungal sporulation was identified in about 1960 in a variety of popcorn. It was inherited by a single gene referred as Ht1. Plants with this gene may have poor horizontal resistance allowing successful invasion but prohibiting the spread from the infected leaf tissue by spores became a major factor in controlling the disease. Most USA corn breeding programs quickly adapted the use of this gene as crossing in the single gene was a much simpler process than selection for horizontal resistance.
A seed production field in 1979 in Indiana, planted with a Ht1 inbred was found to have multiple susceptible lesions caused by this fungus. After being identified in that field, similar reactions were found in several locations that summer in the Midwest. The fungus had a gene that overcame the single gene resistance in corn and produced normal susceptible lesions, sporulating and spreading to others. This became known as Race 1 of Exserohilum turcicum. Other single genes for resistance have been identified (Ht2, Ht3 and HtN) and likewise so has races of the fungus been found to overcome these individual genes.
This is not a new lesson. Single gene resistance, especially one that restricts pathogen reproduction puts considerable selection pressure on the pathogen to favor the variants that can overcome the resistance.
One of the more recent ‘new’ corn diseases was first noted in USA in 2016 is bacterial leaf streak caused by Xanthomonas vascicolapv vasculorum. This disease was known in South Africa since 1949 but in its first year of identifying in the USA, it was seen in several counties of Nebraska and Iowa and Illinois. There are indications that it was also seen in Argentina in that same year. If it was distributed by seed from South Africa, why did it suddenly appear in so many places in one year? This bacterium is a variant of a more common plant pathogen, Xanthomonas campestris. A recent publication by U. Nebraska plant pathology extension
(https://cropwatch.unl.edu/2019/bacterial-leaf-streak-corn-nebraska) listed 16 common grasses in the areas that also host the bacterial leaf streak pathogen. Did the outbreak develop as a mutant of another variant of this species, infecting grasses and building up sufficient intensity until brought to the attention of plant pathologists? Perhaps continuous corn cropping, limited tillage and hybrid susceptibilities also contributed to the ‘sudden’ appearance of this corn disease.
It is frequent that we are surprised by a new distribution of a corn disease and analysis of the cause of the change is often difficult. Genetic variation of pathogen, adaptation of new corn varieties, susceptibility of other hosts, distribution of insect vectors, change in environments including weather and farm culture practices are all potential contributors to distribution changes. Movements of the pathogen can occur with wind, infected seed, grain shipments, equipment movements and even people clothing can be factors. All of these potential contributors probably could account for the initial introduction of a new pathogen and generally goes without knowledge for a few seasons before intensity is sufficient to get attention. After initial identification and understanding significance, breeders can select sufficient resistance to overcome the worst effects of the ‘new’ disease.
I think every corn disease that was identified in the last 47 years of my experience was not first found in only a single location but in multiple locations the same season of initial identification.
Extreme variation in weather patterns in recent weeks in temperate zones worldwide will have an effect on corn plants development resulting in new disease pressures. Southern hemisphere crop has been delayed in harvest because of excessive rain, allowing more time for ear rotting fungi to grow. Northern hemisphere crops have been exposed to unusual temperatures and rain, causing delays in planting, new opportunities for pathogens with swimming spores, and increased distribution of bacterial and fungal pathogens. Corn Journal blog written in September 2018 seem appropriate for July 2019. Is this a new pattern?
Variables affecting corn leaf disease damage nearly always involves moisture and temperature within a corn growing region during a critical corn growth period. Moisture of debris from a previous corn crop is usually critical to spore production by potential pathogens causing many leaf blights. Very slight air movement within a field is sufficient to move spores of many pathogens the short distance from the soil surface to young plant whorls where moisture is usually available, allowing germination and penetration into the leaves. Further distribution from the initial infection can be associated with gentle winds associated with rain storms. Violent storms with hail cause physical damage to leaf tissue, allowing entrance of some pathogens such as the cause of Goss’ Bacterial wilt. Long distance distribution of pathogens is often associated with direction of storms as spores of some pathogens are easily carried in these winds. Pathogens dependent on reproduction on living corn plants are moved from those areas to more temperate zones by storms.
Air temperatures during the corn growing season affects corn leaf diseases as well. Warm and dry environment general inhibits fungal spore production. Cool evening temperatures are usually associated with dew forming on corn leaves, providing the moisture for germination of fungal spores and penetration of the pathogen into the corn leaf epidermis. Warm and humid summer evenings is ideal for some pathogens like Cercospora zeae-maydis, cause of gray leaf blight. Frequent rain favors the spread and infection of pathogens such as Exserohilum turcicum, cause of northern leaf blight.
Vectors of virus diseases are also affected by weather as aphid intensity is associated with drier weather. Corn flea beetles, vector of the bacteria causing Stewarts Bacterial Wilt, movement from environments where the bacteria are maintained on other grasses to new corn planted as the soils warm. Distribution of the insects are often affected by direction of wind.
Annual fluctuations in weather not only affect a corn variety’s physiology and resulting grain production, but also the significance of resistance to a specific disease. A variety may be regarded as adequately resistant to a specific pathogen when under usual low intensity of that pathogen but inadequate when the weather factors change. If we are entering into a period of more erratic weather patterns, we should expect some surprising vulnerability of some varieties to diseases. Corn, as a species, appears to have adequate resistance within its genetics to any pathogen, but it requires time and effort by many people to identify the cause of a new disease occurrence, to identify the source of resistance and incorporate the resistance into productive corn varieties.
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.