The biology of the corn plant after the initial ten days of movement of glucose to the developing kernels is consistent with nearly all hybrids. This Corn Journal blog of August 2016 applies even in the USA Midwest wild summer of 2019.
As the corn embryo develops, and the cytokinins accumulate in the pollinated ovule after the first 10 days, there is a constant translocation of sugars to each kernel for each day. The total daily movement continues for about the next 40 days, almost regardless of daily variable rates of photosynthesis due to cloudy weather or leaf damage from disease. Sugars are drawn from all leaves and even those stored in the stalk pith tissue. The total draw to the ear is determined by genetics of the variety, environmental factors including minerals and the number of kernels. The number of kernels is also determined by genetics and environment factors such as minerals and especially water available during ovule formation and pollination.
The daily transfer of sugars during days 50 to 60 of grain fill is greatly reduced until the abscisic acid affect causes thick cell walls to form at the base of the kernel, cutting off the sugars transfer into the kernel and the movement of water from the kernel. This is known as the black layer.
Sugars translocated to the ear are sugars not available to other living tissue in the plant. Roots are especially dependent on the same sugars to support metabolism functions, including warding off the potential microbe invaders. Starving roots, as they rot, eventually reduce water uptake and, if insufficient water to meet the transpiration rates from leaves, a permanent wilt will occur. With the wilt, movement of sugars to the kernels is stopped, abscisic acid takes over, causing the black layer to form a base of kernel. The consequence is light grain weight on the affected ear.
Two major hormones in corn are cytokinins and auxins. Cytokinins affect cell division and auxins affect cell elongation. Cytokinins are produced primarily in root tip meristems and transported via xylem to other meristems such as those developing in each pollinated ovule. As these embryo meristem cells divide, the attraction of cytokinins increases. Concentration of cytokinins in these meristems also affects translocation of glucose molecules to each developing embryo, as this carbohydrate moves through the phloem from leaves and stem pith tissue to the new cells. Excessive stress affecting water for xylem transport, or, reducing sugar production can reduce the constant flow of cytokinins to developing kernels. If this occurs during the first 10 days after pollination, another hormone, abscisic acid (ABA) accumulates at the base of the ovule. This hormone causes development of thick-walled cells, blocking transport of cytokinins and sugar into the kernel. As a result, the kernel does not develop further.
Genetics and environment have a great effect on the balance of hormones during corn grain development.
Corn shoot apical meristem is genetically controlled to switch from producing new leaf and cells to the terminal male flowers of the tassel. The main environmental factor influencing this switch in temperate zone corn is heat energy. Earlier maturing corn requires less heat to trigger this change in apical meristem products, allowing corn to mature in short seasons far from the tropical environments of corn’s origin.
Plant height is determined by the number of cells produced by cell division at the apical meristem before switching to producing the cells that becomes the tassel and the elongation of the cells. Elongation of the stem cells is enhanced by water pressure applied to the young cells before maturing with less flexible cell walls. Thus, water availability to the roots, root volume and transport of water to the expanding cells in upper plant also affects the eventual plant height.
Corn planted later than normal in temperate zones, accumulating heat units quicker than usual, produce fewer stalk cells because apical meristem is induced to produce tassel cells quicker. If water availability for cell expansion is less than optimum, the result of these two factors will be shorter plants than usual for a hybrid.
Time from germination to production of pollen in temperate zone corn is determined by amount of heat per day after germination. The shoot apical meristem produces leaf and stem cells until it gains the hormonal signals to switch to producing the tassel cells. This occurs while the growing point is surrounded by the growing leaves usually at about the V6 stage. The 2019 rain during April and May delayed planting much beyond normal. Pollination in most fields in Northern Illinois is at least two weeks later than normal.
It will be interesting to see if warmer temperatures after planting this season will cause earlier initiation of the shoot apical meristem to tassel cells and consequently fewer leaves. We attempt to characterize hybrid maturities by daily heat units, with heat units to flowering and/or heat units to abscission layer formation in kernels but actually it is mostly determined by heat for apical meristem differentiation. Time from pollination to completion of grain fill as the abscission layer cuts off translocation of carbohydrates to the grain is mostly a time factor of about 55 days. Consequently, the heat from planting to shoot apical meristem differentiation is the most critical factor on determining when these late planted corn fields will have completed grain fill.
The 2019 corn season in much of the northern USA corn belt will be remembered as distinct from previous season.
We are often surprised when a new (to us) race of an established corn pathogen is found or when a pathogen is found in a new area. It becomes reported as new, but it is highly probable that it had occurred in past seasons but was not found and identified by someone to realize that it is distinct.
Having inoculated disease nurseries with common pathogens near other nursery plants for multiple years, it was always notable to me that the fungal blight was usually not seen elsewhere in the same field. The northern leaf blight fungus, Exserohilum turcicum, produces spores in 2-3 weeks after first infecting the leaf. Those spores from those lesions blown to damp leaf tissue to allow new infection will not produce more spores for another 2-3 weeks. Most corn environments do not provide the needed moisture for continual new infections when the beginning one started at the V8 stage of corn growth. The discovery of the new race in a seed field in Indiana probably was aided by frequent movement in the field by machinery and people plus a susceptible inbred. The fact that after first identified it was found by several specialists scattered across many areas of USA the same year suggest that it had existed for a several seasons slowly building in intensity.
I recall seeing a field in Southern Minnesota that was heavily infected with the fungus Kabatiella zeae causing eyespot that was mostly limited to the area of the field that was in corn the previous year. Apparently, the minimal tillage for the previous season had resulted in large loads of inoculum to infect the new crop but spores had not spread sufficiently to adjacent fields to be noticeable.
A major factor in spread of new fungal pathogens is initial infection, probably not noticed by humans for a few years but eventual increase with minimal tillage and continuous corn growing in the same field. Continuous crop growing is associated with root worm vectored Maize Chlorotic Mottle Virus, one of the components of the corn lethal necrosis in Nebraska and Kansas.
Some pathogens are spread over long distances by wind. Rust fungi, Puccinia sorghiand Puccinia polysoraspread north into the central corn belt by winds. Vectors of viruses are spread by wind as well.
Genetic diversity available within Zea mayshas always provided adequate resistance available to corn breeders within a few years after a new pathogen is identified. Early detection is important to preventing significant damage to the crop and altering the cropping system can be a significant immediate control.
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.
Ht1 gene for resistance to Exserohilum turcicum, cause of northern corn leaf blight, was incorporated in most US hybrids during the 1970’s. This gene was responsible for reacting to initial infection by this fungus by producing a toxin to the fungus in the area of infection that prevented the fungus from producing spores to spread the disease to other plants within the field. In 1979, it was reported that a seed field of corn with that gene had been attacked by E. turcicum producing lesions with spores. Inspection of fields in many locations in the USA discovered the same phenomenon. A gene in the fungus, apparently not previously frequent among the genome, was greatly favored over those variants of the fungus with limited production due to the Ht1 gene in corn, had built up an intensity until it was noticed by the right humans to identify the new race.
This type of genetic battle between host species and potential pathogens is continual. Most potential pathogens are controlled effectively by resistance mechanisms in corn either intentionally by corn breeders screening for resistance when the crop is intentionally exposed to the pathogen. Most damage occurs when new environments favor a variant of the pathogen that allows it to overcome host resistance systems. It is probable that the pathogen variant occurred for several seasons only to gradually build up intensity to be noticed and identified.
Corn Lethal Necrosis, also known as Maize Lethal Necrosis, develops into a damaging corn disease when Maize Chlorotic Mottle Virus (MCMV) and another virus infect the same plant. Both viruses have separate insect vectors. Although MCMV had not been found in the USA until the outbreak of damage from the disease, it was later found that this virus was found in multiple locations, but absence of other viruses prevented notable disease development.
Race T of Bipolaris maydis, cause of the epidemic of southern corn leaf blight had a gene that attacked the mitochondria associated with male sterility of corn. The bacterium causing Goss wilt probably is a mutant of a common grass pathogen. Pathotype 4 of Bipolaris carbonum, cause of very minor pathogen of corn, had a gene that specialized in attacking a common inbred used in many corn hybrids.
There are multiple examples in the many places that corn is grown where the genetics of the pathogens, the corn and environments result in development of what appear to be new diseases. In all cases, efforts by corn specialists identify these factors and reduce the damage by selection of resistance and/or changing the environment that favors the pathogen.
There is no reason to believe that this will not continue. We benefit from the broad genetics in Zea mays.
The 2019 early corn growing season will probably feature unusual disease movements. Having personally seen many of the diseases shortly after being first identified, I do often reflect on how they got there. Eyespot was first identified in Japan in 1959 but more than 10 years later it was found in North Central USA, Argentina, Brazil, Europe and New Zealand. Was it a minor pathogen (Kabatiella zeae) so weak on corn that it only became noticed after more susceptible inbred like Wf9 and W64A became widely used?
Goss wilt bacterium, Clavibacter michiganensis sp. nebraskensis, was first identified in Nebraska in 1970 where it was especially virulent on some genotypes. Switching to more resistant hybrids quickly reduced the damage but the disease was later found in several states. These pathogenic bacteria were found to overwinter in diseased corn debris but how did it spread?
Corn Lethal Necrosis (also known as Maize lethal Necrosis caused by a combination of Maize Chlorotic Mottle Virus MCMV and either Maize dwarf Mosaic virus or Wheat Streak Mosaic virus was first identified in 1976 in Nebraska and Kansas. The virus had been identified in Peru in 1974. Since then MCMV has been found in Argentina, China, Thailand and central Africa. This virus is transmitted by beetles and thrips. Severe symptoms show only when MCMV plants are also infected with the other viruses. Seed transmission has been shown at an extremely low rate. Resistance has been identified.
Damages races of more common corn pathogens such as race T of Bipolaris maydis, Races 1 and 3 of Bipolaris zeicola, Race 1 of Exserohilum turcicumall were related to use of specific
susceptibility genes. Grey leaf spot became notable as susceptible genotypes became widely used combined with less crop rotation and more previous crop debris.
Bacterial Leaf Streak, caused by Xanthomonas campestris pv. zeae, was first identified in Nebraska in 2016. Previously it was only known to occur in South Africa. Is has since been found in 7 USA State and probably in Argentina. Was it always in these areas as a minor pathogen of other grasses but environment and host susceptibility allowed it to increase sufficiently to be identified? Tar spot has been recently noted in north central states after previous identification in higher altitude South American areas. Caused by synergism of two fungi species, much is still be learned about the disease.
There remains much to be learned on mechanisms of susceptibility, environmental factors and movement of pathogens involved in occurrence of ‘new’ corn diseases. It is a non-ending problem in a widely grown crop.
Midwest corn belt planting delays will affect more than only normal yield dynamics but also corn diseases. Corn escapes damage from viruses such as maize dwarf mosaic because the damage occurs when the virus reaches the growing point before the v6 stage of development. Spread of the virus via aphids usually is limited close to the overwintering source of this virus as the aphids tend to spread further north as the temperatures become warmer. Although the June temperatures in the Midwest in 2019 have been cooler than normal, it seems reasonable to assume the aphids can feed on corn at very early development stages further north than usual. Frequent rains could mitigate this aphid survival affect, however. Other virus vectors likewise may have unusual distributions onto corn young plants.
Fungal leaf diseases, such as northern leaf blight, are usually favored by wet conditions. Sporulation on corn debris from the previous year is encouraged by the frequent rain, water in leaf whorls and high humidity allows quick invasion of leaves in the young plants. A few weeks later these lesions become sources of new spores that are easily distributed by winds to new fields. The dynamics of having later planted fields nearby could produce unusual northern leaf blight pressure, especially on those fields.
Gray leaf spot fungus also produces spores on infected leaves from the previous season, but infection of new crop is more favored by humidity than rain. Will excessive rain in June result in higher humidity than normal for the summer of 2019?
Common Rust and Southern Rust spores are carried in storms originating in the Southwest and Caribbean Islands. Corn is most vulnerable before flowering, as the leaf whorl provides an inoculation chamber for the spores to germinate and infect the leaves. The mix of planting dates within an area increases the potential for damage to the later plantings.
This unusual planting season will provide new disease pressures on corn that will require special attention this summer.
Excessive rain in much of the USA Corn Belt in 2019 with ponds of water in areas of fields can encourage infection by a fungus that has swimming spores. Corn Journal blog of 05/30/17 may be appropriate for this year as well.
One of the effects can be infection by an organism called Scleropthora macrospora. This is a fungus-like organism belonging to a group of organisms called Oomycetes. Also in this group are pathogens causing Downy Mildew and Pythium diseases of corn and other plants. Common among these are the ability to form thick walled spores to withstand stress environments that can release swimming spores when in water-saturated soil. S. macrospora infects more than 140 grass species in addition to corn.
The source of infection of corn is often grasses near a low spot or edge of a field. Oospores in the flooded living and dead leaves release swimming spores (zoospores) when close to the corn submerged leaf tissue these zoospores release a germ tube that infects the plant. The filaments (hyphae) grow towards the meristems throughout the life of the plant. This can initially be seen as fine stripes in the leaves but the most obvious symptom is proliferation of leafy aberrations of the tassel- the crazy top symptom. Scleropthora macrospora also can grow to the ear bud meristem, causing similar multiple ears from a single node- but no grain.
Related oomycetes occurring in warmer, subtropical and tropical environments can cause similar symptoms. These downy mildew diseases can also cause the proliferation of the tassels and ears. Susceptible genotypes can have severe grain loss from these diseases. Scleropthora macrospora infection is usually limited to a very small area near grass in a low part of the field.
Infection occurs when the plants have less than 6 leaves. Symptoms that show late in the season, but the problem began with excessive rain that occurred only a few weeks after planting. That early moisture that may contribute to large yields can allow this pathogen to form these unusual corn structures in a few spots of the field. In addition, it is just part of the interesting biology of corn.
Much of the 2019 corn growth in the USA is erratic due to wild swings in water and temperature, affecting planting timing and plant densities. And that is only what we see! Internally many interactions are also occurring and are affected by these environments.
Much of the above-ground growth for the first 30-40 days after seedling emergence is due to cell elongation within leaves. This not only allows the expansion of leaf blades to increase the mass of leaf tissue, but also elongation of the leaf sheaths, pushing up the plant height. Cell elongation is not only occurring in the outer tissue, but internal cells also grow in size during this time.
Cell elongation is driven by energy allowing production of cell components such as cell wall cellulose and lignin but also increase in the membranes, ribosomes, mitochondria and chloroplasts needed to drive the growth. Immature cells, before tightly constricted by deposits of solid cell walls, expand with water pressure during this growth pressure. Consequently, soil water and root development become major factors affecting the size of the corn plant during this pre-flowering stage. Root development not only affects the absorption and movement of water into these growing leaf cells but also uptake minerals needed for the general metabolism. Expansion of leaf blades during this time also increases the absorption of light driving photosynthesis, providing more energy for cell function and growth.
Multiple environment factors influence water supply to corn plants, but genetics also distinguish variety reactions to growth of the plant. Root size and growth pattern affect water and mineral uptake. Structure of vascular tissue from roots to leaves affect efficiency of water movement. Number and activity of stomata in leaves affect the evaporation of water from leaves. Efficiency and number of chloroplasts within the cells affect the transmission of light energy to carbohydrates, mitochondrial numbers and efficiency affect the change of this energy into ATP for use in the formation of proteins and other products needed for cell growth. Translation of chromosomal DNA to RNA that moves to ribosomes where the codes for specific amino acids are strung together for specific proteins, some of which are used as enzymes driving production of cell structure components. A large number of those 30-40000 corn genes must be participating in that early growth of a corn plant.
It is difficult to predict the final grain production of fields under these circumstances and it is probably that all hybrids will not react the same, even if the principles of biology will apply to all.
After emergence and successful elongation of the first true leaves, photosynthesis becomes the energy source for future growth. Consistent with its tropical origin, corn photosynthesis is negatively affected by low temperatures. Leaves grown at 14°C (57°F) have 30% of the photosynthesis rate as those grown at 25°C (77°F). (Plant Physiol. (1995) 108: 761-767). Much of this reduction is recovered within a few hours if the leaves are returned to the higher mid-70 temperatures.
Light energy absorbed by chlorophyll causes an electron to be moved within the chloroplast but if it does not ultimately get utilized in synthesis of carbohydrates, it can damage a critical protein needed in photosynthesis. Corn chloroplasts react by producing a yellow pigment (zeaxanthin) protein that is active in the quick recovery after the heat returns. Chlorophyll molecules are relatively unstable especially in high light intensity and low temperatures, further contributing to reduced photosynthesis at the lower temperatures.
Another protection system in corn, and other plants, that develops in the cell outside of the chloroplast is the pigment anthocyanin. This red pigment absorbs the blue light spectrum of sunlight and thus reduces photosynthesis. Anthocyanin forms after the sugars reach a high concentration. This often happens in seedlings when sugars are unable to be translocated to the roots, again because lack of the heat energy needed to move the sugars. Hybrids vary in the tendency to produced anthocyanin, occasionally causing alarm to the grower but return to warmer temperatures results in disappearance of the red color and normal photosynthetic rates in the seedling leaves. (Corn Journal, 5/5/2016)
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.