It is corn harvest time in the Northern hemisphere. Benefits of genetic diversity in this species becomes increasingly evident at harvest time. Grain yields vary among the hybrids and environments. Differences were the culmination of the multiple genetically influenced morphological features. Roots that extended deep in the drier environments provided access to more water, increasing the turgor pressure for silk elongation during the time of exposure to pollen. On the other hand, if the post flowering environment was extremely wet this tap-rooted hybrid type could be vulnerable to root lodging. The hybrid with shallow, branching roots favored in organic rich soils favored by frequent rain during the season, may not have had enough turgor to push out these silks during much of the pollen shedding time, harming the grain yield.
Leaf size and shape differences were factors in photosynthetic rates among hybrids. These morphological features interacted with plant density, fertilizer and sunlight intensity of the summer to affect carbohydrate production by the plants. Leaf disease resistance affected net photosynthesis during the season. Genetic differences among hybrids for reaction to accumulated heat influenced the timing of pollination. Longer time to flowering allowed for more accumulation of carbs in the stalk and more reserve for grain fill if late season stresses reduced photosynthesis. Genetically influenced differences in vascular tissue structure affected the rate of movement to sugars to the grain. Varieties differed in hormone influenced rate of movement to each kernel. Duration of sugar translocation after pollination was also affected by genetics. Ability of roots to maintain life when under the competitive pressure from grain filling was another difference among hybrids.
Kernel feature differences become visible, especially to corn breeders as they harvest nurseries. Endosperm texture differences are evident. Yellow colors vary in intensity, with simply inherited traits such as blue, red and white endosperms being most extreme. Shape and length of the ear are inherited traits contributing to the grain yield and drying characters of the hybrid. Less obvious genetically influenced character such as pericarp thickness are important to grain drying after formation of the abscission layer at the base of the kernel. Genetics affected the number and length of husk leaves surrounding the ear. This affected protection of grain from pests but also field drying of the grain.
As we observe the diversity of corn genetics we should appreciate that 8000 years of human interaction with this species as resulted in a diverse crop adapted to multiple environments across the earth. Each season, in each field, may favor different specific genetics but diversity is the key to the long-term success of this efficient converter of light into useful stored energy.
This corn disease has become evident in areas of northern Midwest corn states of USA in 2018. Although the disease has been known to occur in specific areas of Central and South America for many years, its first known appearance in the USA was in 2015. I saw it in our plots in Northern Illinois in 2016 but it was only on a few plants. Spread and intensity on most of our nursery in 2018 was surprising. It appears to be in most fields in the region late in the season. This disease occurrence raises many questions about its significance to effect on yield and stalk breakage vulnerability. Answers will depend upon understanding the interaction between the fungus (or fungi) biology and that of the corn.
The fungus (Phyllachora maydis) is believed to be an obligate parasite of only the corn species. This implies that it can only grow and reproduce in living corn tissue. It has not been shown to be transmitted in corn seed. Phyllachora maydisis only known by its sexual reproduction stage. It belongs to a group of fungi called Ascomycetes identified by production of haploid spores in elongate mycelial tubes called asci after the fusion of spores. Many corn leaf diseases are caused by Ascomycetes but most of these pathogens reproduce asexually as conidia. Most also cause initial infection with these conidia being produced on infected dead leaves. Have we misunderstood this potential in this fungus?
It is currently unclear how this pathogen is interacting with corn. Our PSR corn disease nursery includes many inbred and hybrid entries from US seed companies. We inoculate these with 5 pathogens to evaluate resistance as a service to the companies. Most are not identified to us by hybrid or seed parents, but it is assumed they represent a range of genetics and maturities. I observe plots frequently during the summer but missed the early development of tar spot. I did not record seeing the disease until at least 2 weeks after most plants had flowered. Increase of symptoms was dramatic. It also appeared to be related to rapid increase in gray leaf spot and leaf senescence. These confusing apparent interactions of senescing leaf tissue increase in gray leaf spot and tar spot has continued.
Many corn researchers are now working to resolve questions brought about by this 2018 observations. Where did the inoculum originate? From infected debris of past year, seed or spores blown in from Mexico? What was the environmental influence that resulted in the disease outbreak? How to identify resistance if artificial culture of the pathogen is impossible? How to distinguish resistance from maturity differences? Does Phyllachora maydiscause do significant damage to the plant or is it only significant when combined with other leaf pathogens? Does the pathogen produce a phytotoxin resulting in death of leaf cells?
I suspect these questions will not be easily or quickly resolved. Biology of this pathogen, interaction with corn plant and environmental influences are all involved in the complex.
U.S.A. Midwest farmers are seeing more stalk rot this year than most years. Weather during the growing season is the most likely the cause. Early season moisture established good growing for much of the corn growing areas. Rain was more than average for many areas, although others were excessively dry. Most of the summer was warmer than normal as well. Plants responded to the heat by moving to flowering quicker than in some summers. Extra water resulted in more shallow roots but also good extension of the silks and high kernel numbers. Weather after flowering also varied with warmer than normal temperatures, high humidity and scattered rain showers in much of the upper Midwest.
Humid warm nights favored the fungi causing gray leaf spot and tar spot. Areas with frequent rain during the month after flowering developed significant northern leaf blight on corn. Each of these diseases destroyed significant photosynthetic tissue in susceptible corn hybrids. Weather during that period also tended to be cloudy, reducing the rate of photosynthesis. Warm nights increased the cellular respiration rate more than the cool Midwestern nights that are more common in these areas. 2018 summer weather in much of the US corn belt resulted in high kernel numbers, photosynthetic stress after flowering due to leaf disease and cloudy weather. Competition for use of reduced levels of sugar between translocation to the kernels, and cytoplasmic respiration in all plant tissues frequently resulted in degradation of roots and eventual root rot. This was followed by plants wilting. Many fungal species invaded the dying stalk tissue created the obvious symptoms of Fusarium, Gibberella, Diplodia or Anthracnose stalk rots.
Hybrids that showed a high incidence of stalk rot in 2018 probably would have been OK if this specific weather pattern had not occurred. Correctly predicting the 2019 weather will be helpful in deciding on the best hybrid, tillage, plant density and other inputs for that season. This is not an easy task.
Assigning a name to the dominant fungus in a rotting corn stalk implies that an aggressive pathogen attacked the plant and therefore caused the plant to be vulnerable to lodging. Symptoms of black streaks on outer rind indicates that the problem was anthracnose, caused by Colletotrichum graminicola. Small dark pycnidia emerging from rind tissue near the node indicates that Diplodia maydis was dominant. Perithecia of Gibberella zeaeon surface of rind and pink color inside the rind of the lower stalk suggests that this was the main cause of the rot. Fusarium verticilloidesis always present in rotting stalks and therefore can be assigned as the cause if none of the above symptoms are present.
It may be comforting to assign a name for the stalk rot, but it can lead to avoiding the more difficult analysis of the actual cause of the plant dying before normal completion of grain fill. The predisposition of the stalk to invasion by any of these fungi involves the complex biology of that corn plant as it moves available sugar to the grain. If the plant did not supply enough carbohydrate to meet that demand, root tissues became deficient of the metabolic energy needed to fend off the multiple soil organisms capable of invading and digesting weakened root tissue. Similar deficiency in lower stalk tissue likewise decreases resistance to the many fungi, including those named above. If roots are sufficiently damaged that water uptake cannot keep up with water loss from transpiration from the leaves, the plant wilts. This further weakens the stalk as the pith tissue withdraws from the rind, changing it from the strength of a rod to that of a tube.
Although the fungal related cause of the stalk rot may be easy to analyze, the more important analysis should involve the basic reasons that the plant did not reach the season with sufficient sugar to maintain root and stalk living tissue until completion of grain fill. Did a leaf disease result in reduced photosynthesis? Did early season environment factors, such as water supply cause better silk emergence than normal for that hybrid but late season stress such as lack of water or cloudy weather reduced photosynthesis? Was the plant density too great for that hybrid for that season? Nitrogen-potassium ratio was wrong for that season? Best hybrid for the previous season may not have been the best for this season and, likewise, the one that had stalk problems in a season with more stalk problems may be the best the next season.
It is good to analyze for potential causes of stalk rot in the field when it occurs, harvest before severe lodging and then put together the potential causes of insufficient photosynthesis to meet the translocation demand to the ear without causing excessive root tissue death. Having a name for the obvious stalk rotting fungus may seem comforting but getting at the main biological cause can lead to reduced problems in the future.
I first was introduced to corn diseases in 1971, when asked to identify diseases on corn leaves gathered across the US, Race T of southern corn leaf blight was still a potential problem. Although my master’s degree in plant pathology from Kansas State University was helpful, my PhD at University of Tennessee emphasized botany and mycology (study of fungi). That disease resulted in seed corn companies deciding that they needed to add a plant pathologist to their research program. So, when asked, I told them that I was one. The withdrawal of T sterile cytoplasm from corn solved a significant disease problem at that time. Corn breeders for the company then asked if I could help solve the problem with corn stalk rot. A search of research literature showed that stalk rot had been studied by many in the 1960’s. Perhaps, the fact that this coincided with increased use of single crosses is significant because it made it clear that individual plants with near identical genetics did not show the same degree of stalk deterioration. Researchers studied cell death in stalk pith cells, reduced sugar levels in stalks were associated with stalk rot. Others showed that root rot generally preceded stalk rot. Although some fungi such as species of the genera Diplodia, Gibberella and Fusarium were obvious in rotted stalks, multiple other species of fungi were also present. I presented that literature in a summary to a group of corn pathology researchers in 1975 (a copy listed below).
Corn plants are most vulnerable to premature wilting during the period of 40 to 60 days after flowering. This sudden change in the plant appearance is due to depravation of sugar to roots because of competition with grain in plants with insufficient photosynthate to meet metabolic needs of the roots and the translocation pull to the grain. Each factor is a complex genetically involving physiology of photosynthesis, morphology and disease resistance of leaves, root structure, rate of translocation of sugars to each kernel and number of kernels. Environmental influences such as plant spacing, moisture influencing kernel numbers, daily light intensity and pest and disease pressure.
Wilting, commonly known as premature death, occurs scattered within a corn field as majority of plants maintain normal green and turgid leaves as they continue to move sugars to the kernels while maintaining enough root tissue functions for water absorption and movement to the leaves. The wilted plants show the outside appearance of gray leaves and ears turning downwards. Wilting causes major internal changes in the corn plant. Physical strength of the stalk is reduced by 1/3rd as the pith tissue is withdrawn from the outer rind tissue, essentially changing the strength of a solid rod to that of a tube. This is even before fungi begin to digest the cell walls of the stalk. Most cell metabolism is halted within a few days because of dependency on water. This includes translocation of sugars to the kernels, resulting in light kernel weight, compared to kernels on plants that continue to function for the usual 60 days after pollination. Kernels of affected plants form an abscission layer (black layer) within a few days after plant wilting although kernels on most non-wilted plants delay the abscission layer formation until normal grain fill is finished.
Individual plants with wilting symptoms have lighter kernels than most plants in the field because of this shortened grain filling period. If these plants did not have unusual environmental stress such as leaf disease or insects causing upper stalk breakage, they probably had more kernels than the adjacent, green plants. A study published in 1980 (Phytopathology 70:534-535) showed that wilted plants with no obvious leaf damage had 10% more kernels than adjacent non-wilted plants. The individual plants may have nearly identical total grain weight, depending upon the timing of plant wilt in relation to normal grain-filling period. A few wilted plants within a field can indicate that near maximum yield was obtained for that hybrid in that season’s environment. However, the ensuing effect on lodging detracts from that optimistic view and is the subject of the next Corn Journal issue.
Sugars produced in pre-flowering corn plants supply the basic energy and carbohydrates for root growth and metabolism just as photosynthesis provides similar tasks for leaf and stalk growth. Hormones such as cytokinins produced in growing points are linked to the movement of sugars to the above and below ground parts of the corn plant. Roots are hard to study but research has shown corn root size begins to detract about 10 days after flowering due to root rot. This rotting can be gradual and may have no above-ground visual effect.
Movement of sugars to newly formed kernels is slow for the first 10 days after pollination, with 80% of the deposit occurring during the next 40 days, at the rate of about 2% of the total per day. That movement is linked to the hormone production associated with each new embryo in the ear. This pull to the ear is constant during that period regardless of reductions in photosynthetic rates due to cloudy weather or leaf disease. Sugars come from other sources such as those stored in the corn stalk pith cells. It also becomes a major competitor with the root cells in need of the sugars for the metabolism to prevent invasion by the multiple microorganisms in the soil with enzymes to destroy root tissue.
If the reduction in photosynthesis during this grain fill period is drastic and is combined with a large pull of sugars to the developing kernels, root destruction by pathogens can cause sufficient interference with uptake and transportation of water to the leaves. Failure to replace water lost by transpiration, causes the plant to wilt. A plant with bright green, turgid leaves suddenly turns gray in color and limp in structure.
An extreme example of the stress of too strong of movement sugars to the ear is observable in the outer row of a corn field where those few plants with 2 fully-pollinated ears show early wilt symptoms. In the canopy of the field, those wilted plants will either have more kernels than adjacent plants and/or show some signs of reduced photosynthesis such as borers causing upper leaves to be removed, leaf damage from foliar disease or uneven spacing allowing shading from adjacent plants.
There are genetic factors influencing root structure, number of kernels, amount of sugars translocated to each kernel, photosynthesis rate per plant and reactions to environmental stresses. Early wilting of plants not only allows the progression of fungi associated with stalk rot but also directly weakens the strength of the stalk.
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.
Distribution of the two main corn rust diseases, common rust, caused by Puccinia sorghi and southern rust, caused by Puccinia polysora, is closely related to origin of storms. Both of these fungi are obligate parasites, producing spores only on living plants. They have complex life cycles involving other spore types but the asexually produced urediniospores are the primary means of the spreading of the disease.
Puccinia sorghi, despite the Latin name, only infects corn (not sorghum), and thus temperate zone corn must receive urediniospores from where corn is grown in subtropical areas. In the USA that is usually in Mexico. Urediniospores are small single cells with a thick wall that delays desiccation when carried by high altitude winds. Storms during month of April-June often originate in the Southwestern regions of the country, moving across Central corn belt states. Urediniospores require about 6 hours of moisture to germinate and penetrate the corn leaf. This is the environment of the corn leaf whorl during these months, allowing early establishment of the disease in a field. More spores are formed from this initial infection within 7 days, allowing more local spread. Timing of infection is significant because of continual moisture present in the whorl. If storms carrying the spores arrived during the early corn growth period, further spread within the field is likely. Late planted corn frequently has more vulnerability to the disease, but timing and origin of storms also is significant.
Urediniospores are orange in color, but spores produced as the corn plant matures are rust pustules producing black teliospores. These will not infect corn but only the alternate host, a tropical Oxalisspecies. That process includes sexual reproduction allowing for meiosis and generation of new genetic combinations of rust. That becomes the source of common rust races that overcome the single gene resistance used in corn. The new races originate in the tropical areas where the rust fungus completes its life cycle, including recombination of its genetics. The new races spread with storms, increasing as they overcome common single gene resistance.
Puccinia polysora has a higher temperature requirement for infection than Puccinia sorghi, but the spread to temperate zone is also affected by storms. Although the alternate host for completion of its life cycle is unknown, genetic variability in the fungus suggests that it does exist.
Whereas many corn disease pathogens are simply dependent on moisture and humidity for disease development, the rusts are also depending on direction of early season storms to spread from tropical to temperate areas.
Cercospora zeae-maydis infection is strongly related to relative humidity. Weather in Northern Illinois in 2018 has provided a prime example of the difference between the dependence on moisture from rain for infection by Exserohilum turcicum, cause of northern corn leaf blight, and that of the fungus causing gray leaf spot. Both fungi sporulate on infected corn debris. C. zeae-maydis spores are considerably lighter allowing further distribution within and outside the corn field. E. turcicum requires some free moisture on the leaf to germinate and penetrate the leaf epidermis within a few hours after germination. C. zeae-maydis depends more on humid air than free water to germinate and grow on the surface of the leaf. Growth chamber experiments showed that penetration into the leaf only occurred after 100 hours of 90-100% relative humidity. It is remarkable that the hours do not need to be consecutive but can occur after a series of humid nights, for example. The fungus appears to have the ability to halt hyphal growth until the next high humidity period.
Most of the midseason weather here this summer has featured little rain but warm humid days and nights. Northern leaf blight is not frequent in corn but scattered gray leaf spot lesions are easily found. This example is typical of occurrence of this disease. Although the disease was known in USA more than 50 years ago, it gained notice in the humid environments of Virginia in early 1980s. Wide use of susceptible genetics allowed spread first to areas around river valleys further west until it had spread to the irrigated areas in western corn belt. The pathogen is now present throughout most areas of USA corn belt, becoming especially noted during warm humid seasons.
Weather during corn growing season affects these two corn pathogens in distinctly different ways. Heavy spores of the Northern Leaf Blight fungus tend to not be carried far by wind whereas the lighter spores of the Gray Leaf Spot fungus are easily moved field to field. Northern Leaf Blight fungus is favored by frequent rain showers, but the Gray Leaf Spot fungus is favored by less rain but warm humid weather.
This corn disease caused by the fungus Exserohilum turcicum should have a different name because it occurs tropical, subtropical and temperate zones in all continents. Its occurrence and severity, however, is greatly affected by weather. Spores (conidia) are produced on moist, infected dead or living leaf tissue in humid conditions. These spores are bigger and heavier than those of some corn pathogens such as the cause of gray leaf spot (Cercospora zeae-maydis) and thus tends to move a short distance within a field. The small percentage that are picked up during strong storms do spread the disease longer distances however. There are instances where the disease will be concentrated in a small area of a field apparently initiated with a few early infections and spread mostly to adjacent plants.
Spore production is encouraged on a moist substrate in a humid environment, but new infection requires the spore to be in moisture for a few hours. Condensation on leaves with cool evening temperatures can be adequate, moisture in the leaf whorl while plant is young, and frequent rain showers are usually adequate for the spores to germinate. These elongate, multicellular spores send out hyphae from cells on each end. The hyphae set up clusters that enzymatically drill into the host epidermal cells to absorb nutrition. At his point the fungus is no longer dependent on weather.
The fungus grows within the leaf towards the vascular bundle. As it feeds and grows in the local vascular cells, a small wilt symptom develops about 2 weeks after initial spore germination. High relative humidity that can be associated stimulates the creation of more spores from the lesion and with rain showers the cycle is repeated.
Occurrence of severe outbreaks of this disease in seasons and locations with frequent rain showers and higher humidity has resulted in natural and intentional selection of higher levels of resistance in some corn-growing regions than others. Open pollinated varieties of the early 1900’s with highest resistance were selected in the Eastern United States. Many tropical varieties tend to have higher levels of resistance than those selected in drier environments.
This disease frequently is more severe in a small region that happened to have frequent rain showers during the corn midseason development. Resistance differences will be more evidence in these conditions than when corn is grown under drier and less humid environments, which may occur in the same field the following season.
Bacteria are single cell forms that continually surround corn above and below the soil. Defense systems of corn, and all other forms of life, generally is effective in keeping potential pathogens from invading cells, while tolerating the saprophytic nature of most bacteria species. Bacteria are vulnerable to desiccation and generally most successful in moist environments, including those inside corn plants.
Corn plant defense systems against bacterial infection includes the tight epidermal layer of cells with a waxy covering that inhibits invasion in leaves. Vulnerability to entrance through stomata is limited by the anti-microbial fumes emitted through the stomata. If this outer defense is avoided, some pathogenic bacteria thrive on the moist internal leaf environment until other host resistance systems stop its spread.
Goss wilt bacteria (Clavibacter michiganensissp. nebraskensis) was first recognized causing a corn disease in 1969. The disease was strongly linked to physical damage to leaves by hail. Breaking the leaf epidermis allowed the bacterial to enter and thrive in susceptible corn genotypes. Spread elsewhere in the USA corn belt has implied that less obvious damage, perhaps from wind in rain storms provide sufficient injury for the bacterial to enter plants. Structural damage to leaves and moisture are essential to successful invasion by this bacterium.
Stewart’s wilt bacteria (Pantoea stewartii) cause corn disease by avoiding desiccation by surviving in an insect vector, primarily the corn flea beetle (Chaetocnema pulicaria). This insect feeds on corn and other grass leaves, penetrating the epidermis while inserting the bacteria into the leaf. This pathogen multiplies and spreads especially through the vascular system in susceptible genotypes.
Bacterial leaf streak is caused by bacterium (Xanthomonas vasicola pv. vasculorum) that appears to invade through stomata. Appearance of linear lesions mostly limited on sides by vascular bundle cells implies that these bacterial mostly digest the mesophyll cells in susceptible genotypes. There are some indications that it is associated with warm, rainy weather, perhaps allowing the bacteria to increase in the moisture of the corn whorl and eventually penetrating through the stomata.
A few other Xanthomonas and Pseudomonas species have been associated with contaminated irrigation water from ponds with infections causing leaf blights. Bacterial stalk rot likewise is associated with heavy concentration of a bacterium (Erwinia carotovora) in flooded soils, allowing penetration in to the lower shoot area of the plants.
Although most corn inbreds and hybrids have good resistance to most of these bacteria, inconsistent weather patterns, genetic changes in potential pathogens, factors influencing vectors and unexpected susceptibility in new corn genetics have and will continue to allow emergence of bacterial diseases.
Apparent changes in weather patterns during recent years affects corn and pathogen biology. Diseases may be more prevalent in areas that they were virtually absent and nearly absent in areas in which they were frequently damaging because of timing of particular weather.
Diseases caused by viruses such as Maize Dwarf Mosaic (MDMV), Maize Chlorotic Dwarf (MCDV, Maize Chlorotic Mottle (MCMV) are transmitted by insect vectors which are also affected by weather. Virus generally must reach the growing point of the corn plant to damage the plant or even show symptoms. Consequently, the infection must occur before the V4 seedling stage before the apical meristem is pushed upwards by cell elongation. Wet weather can delay planting, allowing increasing populations of the vectors feeding on alternative virus host plants such as Johnson grass (Sorghum halepense). As result of increase of aphids feeding on MDMV-infected plants and delayed corn planting, transmission of the virus into corn seedlings allows the virus to become systemic after it reaches the apical meristem. This becomes especially damaging if the leafhopper (Graminella nigrifrons) picks up the MCDV virus from grass hosts and then feeds on the same young corn plant. Synergistic effect of concurrent infection by these two viruses can cause extreme damage to susceptible corn genotypes.
This synergism between two viruses has even be more damaging when a MDMV or Wheat Streak Mosaic Virus (WSMV) infect the same plant infected with MCMV. The result is Corn Lethal Necrosis disease. WSMV is transmitted by wheat leaf curl mite (Aceria tosichella), that frequently picks up the virus from infected wheat. Maize Chlorotic Mottle Virus is transmitted by beetles, primarily Diabrotica species in the USA and by thrips (Frankliniella williamsi) in Africa. Transmission can be done by larvae and adults. Corn plants infected as seedlings with MCMV vectored by infected rootworms (Diabrotica species) and MDMV or WSMV as vectored by aphids or wheat leaf curl mites will be severely damaged. Weather affecting timing of planting of corn, growth or control of alternate hosts such as Johnson Grass, harvest of wheat all interact in determining the damage from these viruses.
Several other viruses, each with unique dynamics of vector biology, alternate hosts and corn development cause significant damage in specific environments. Weather is significant in each development of each of the diseases. Many perennial grasses are infected with viruses and are vectored by insects that feed on both corn and the grasses. Weather affects the plant and insect biology in relation to timing and intensity of virus infection in corn. Infection by one virus species may go unnoticed but dual infections because of the coincidence of many variables can result in considerable damage to corn.
Cytokinins and auxins are operative during all of the corn plants life, including the movement of sugars to the young kernels. These two kinds of hormones have different roles in origin and effect on corn growth. Cytokinins are mostly produced in root tips in root meristems and transported through the water distribution in the xylem tissue. Auxins are mostly produced in stem meristems and distributed in the phloem system. Cytokinins are associated with increasing cell division in the stem meristems whereas auxins are involved in cell elongation. Apical dominance resulting in the corn plant usually having only one upright stem is because of the interactions of the auxins produced in the apical meristem. Removing that stem tip in early corn development and thus reducing auxin production tips the balance towards more cytokinin and stimulation of cell division in the lateral buds of the corn plant, resulting in branches.
Pollination of the multiple ovules in the corn ear results in attraction of cytokinins to each developing kernel. Moisture stress during the first 10 days after pollination is known to cause early death to some kernels, perhaps because of reduction transportation of cytokinins to the most immature embryos (my conjecture!). Cell division in the new embryo meristems establishes the movement of sugars through the phloem to the kernels. Much of the sugar is deposited into the endosperm portion where it is changed to more complex carbohydrates and thus allow the osmotic pressure for more sugar movement towards the kernels.
More is known about the effect of these plant hormones on plant growth than all of the mechanisms involved with those effects. Auxins involvement in cell growth involves softening cell walls, making elongation of cells easier. Cytokinins have been shown to prevent protein breakdown and activating protein synthesis.
Cytokinins produced in root meristems are transported to and stimulate the cell division in the kernel embryos. Meristems of those embryos produce auxins. Auxins are associated with production of ethylene which has been associated with formation of abscission tissue as leaves and fruit mature. It is assumed that the auxins are associated with formation of the black layer at the base of kernels, resulting in stoppage of movement of material to the kernels.
We know that these plant hormones are associated with the growth of corn tissues including the formation of kernels but there remains lots to learn of the actual molecular interactions that allows this to happen. Meanwhile, corn breeders, agronomists and growers attempt to coordinate it all by selecting the genetics that maximize grain production.
Water moves from soil into root tissue by diffusion, going from higher concentration in the soil into the cells with water concentration diluted by sugars and minerals. Each mineral likewise is absorbed according to its own concentration inside and outside of the root cells. Movement of water and the mineral solutes flow upwards because of water cohesiveness and the removal of water via transpiration through leaf stomates.
Minerals pulled along with the water are essential to each biochemical process, from formation of cell components to the function of those components. Not only the structures but also manufacture of products integrate the minerals are dependent upon the supply of minerals carried from soil with water.
Stomatal pores are open during the day as the result of photosynthesis and unique shape of guard cells of the stomates (https://www.cornjournal.com/corn-journal/corn-leaf-epidermis). Evaporation of water through open stomata is determined by relative humidity immediately outside the openings. Transpiration is greatest if immediate outside humidity is low. Water movement from roots to leaves is greatest in a dry daytime environment. It follows that mineral movement from soil to leaves that is greatest with drier daytime environments. This becomes especially significant during growth stages of corn as minerals become tied up in cell structures but some elements such as nitrogen, potassium and phosphorus are essential components of enzymes essential to basic photosynthesis and respiration needed continued cell function until completion of the corn plant’s life cycle.
Among the genetic differences in corn varieties is efficiency of water absorption. These must involve structural differences affecting total roots volume and direction of growth. Some have a deeper root and some more spreading than other varieties. Each may be more suitable for specific soil conditions and a season’s weather. Varieties must also differ in vascular structure affecting the efficiency of movement of water upwards.
Varieties of corn also must vary in number of stomates. More stomates may result in ability to absorb more carbon dioxide for photosynthesis and also more movement of water with minerals from the soil but this advantage may be a disadvantage during drought weather. Variety features such as more leaf area is advantageous for total photosynthesis but may result in higher water loss because of more stomates.
Water and mineral movements are affected by a combination of plant structure and environment ultimately expressed at the end of the growing season by grain yield.
Sugar solubility of water favors the initial movement of water into root hairs. This process of movement of water across root hair cell membranes is a physical phenomenon of osmosis, as water moves from a higher concentration outside the root hair to a lower concentration in the sugar (and other molecules) dissolved in water within the cells. This osmotic pressure also promotes water movement into the xylem tubes within the vascular bundles of the roots.
Water cohesiveness keeping the water molecules together along with the removal of water molecules from transpiration through leaf stomata, essentially pulls the water up the plant, carrying with it the minerals dissolved in the water.
Corn stems and leaves with multiple vascular bundles in the stem contribute to stability of water uptake and distribution throughout the leaves. The veins are parallel to each other in the corn leaves. At the base of the leaf, where it connects to the stem at the node, the system becomes much more complex. The vascular tissue goes horizontal with fusions between the individual veins. Also, the xylem ‘tubes’, (vessels) have end walls, forcing the water moving up from roots and stem through small pores that act as filters. The pores are sufficiently small to filter out any particles being carried upward with the water. Many bacteria and even some viruses are too large to pass through the pores. Each node of corn, even in the small seedling, has this complexity of the vascular tissue. Root vascular tissue connects with the stem vascular system at the first leaf node. Whereas an individual leaf may have up to 20 main veins, the node may have 100 horizontal vascular bundles and with fusion of vessels at the nodes. This redundancy protects the plants from a problem in single vascular bundle or one root branch from blocking transport of water and minerals to the leaves. Likewise, the movement of carbohydrates from leaves to roots gets distributed to all roots. Water soluble substances such as minerals and toxins can move freely up the plant with water through the xylem, but most fungal spores and bacteria are filtered out by the pores.
Movement of water into stem and leaf cells also is physical, water moving from higher water concentration in the xylem tubes through membranes of the living, metabolically- active cells, allowing direct utilization of water in photosynthesis and other activities. Cohesiveness allows more water to follow.
We are apprehensive that corn plants lose water through transpiration but also should appreciate that because of the loss of water through the stomata, not only is CO2 allowed in the plant, and oxygen escapes, the process allows uptake of water and transport of minerals also is occurring.
Water is essential to growth and grain production of corn. It is estimated that current corn hybrids require about 20 gallons of water per plant to produce high grain yields (http://articles.extension.org/pages/14080/corn-water-requirements). Of course, the actual number is variable as affected by weather.
Water is essential for all plants because of its unique molecular structure. Oxygen atom fulfills its need for 2 electrons by sharing an electron from each of two hydrogen atoms. This specific covalent bond with hydrogen is unique in that the single hydrogen atoms are not distributed exactly symmetrically around the oxygen atom, resulting in a water molecule with a slight negative charge on one side of the oxygen component and a slight positive charge around the hydrogen components. This has profound and unique effects on water characteristics essential to plants.
Water molecules are cohesive. They attract other water molecules because each has a slight positive and negative electronic charge. Cohesion of water molecules is essential for the transport of water from the root hairs through the xylem tissue up to stem growing points and leaves. This strong capillary action allows movement water molecules upwards as water evaporates and escapes the plant through the stomata that is replaced by water molecules being pulled upwards.
Water is a universal solvent, again due to its polarity. The negative side of the oxygen atom and the positive side of the hydrogen atoms essentially break apart most ionic compounds. Consequently, it becomes solvent to most mineral sources essential for corn growth. For example, the positive charged potassium ion of potassium chloride is attracted to the oxygen side while the negative side of the chloride ion is attracted to the hydrogen side of the water molecule. This allows the transport of essential minerals for metabolism and structure of the plant.
Oxygen and hydrogen components of water also are essential to the many complex chemical reactions that are within the corn plant cells. Water interacts with the essential storage of energy in carbohydrates during photosynthesis and the release of that energy during respiration.
There are obvious effects on corn when water is deficient but there are also many hidden aspects of the unique water molecules essential to corn growth. An interesting summary of properties of water can be found at https://en.wikipedia.org/wiki/Properties_of_water.
Vascular systems of corn plants include xylem cells that essentially become small tubes allowing the movement of water mostly by then tendency of water molecules to stick together (cohesion). As a molecule is removed from the leaf thru a stomate, one is pulled up from the root. Movement of carbohydrates from the source of photosynthesis in leaves to the various sinks in all living tissues of the plant is multidirectional and complex. Glucose, the immediate product of photosynthesis, is transformed into more complex sugar molecules such as sucrose when it is moved.
Movement carbs between cells can be simple diffusion through those small ‘holes’ in cell walls, the plasmadesmata, as the molecules move from a high concentration to a low concentration. It is a little more complicated with travel through membranes by osmosis, but the basic principle is the same. Water is involved because It is the solvent of the sugar. Greater concentration of water equals less concentration of sugar. Water molecules are also affected by the principles of movement from high to low concentration, setting up dynamics for what is called turgor pressure within each plant tissue.
As the sucrose molecules move into a ‘sink’ such as the newly formed kernels, they are transformed into more complex molecules such as starch and thus maintains the osmotic pressure for more movement of sucrose into the kernels. Other sinks, such as biologically active tissue of all living plant cells, consume the sucrose in cellular respiration and formation of essential amino acids and cell structures. These various sinks are not all in the same direction from the carbohydrate sources where the photosynthesis occurred and consequently flow among phloem cells may not be in the same direction.
Whereas water movement in xylem tissue of the vascular bundles of a corn plant is mostly upwards from the roots, movement of the products of photosynthesis is affected by concentrations of various sugars in the sinks, allowing bi-directional flows.
Sugar is the product of photosynthesis, a process at which corn is especially good. The sucrose form of sugar is moved (translocated) from the photosynthetically-active leaf (source) to sinks such as growing leaves, roots and, eventually, seeds. Hormones, mostly cytokinins, direct direction of the flow. Translocation occurs through the phloem portion of vascular bundles through cell membranes at the cost of some energy. Cytokinins are mostly produced by the newly developing cells at growing points such as tips of root branches, leaf buds, growing leaf tips and embryos in newly formed kernels. We humans selected from the Teosinte ancestor, plants that not only met the minimal needs of producing seeds to assure a future generation but also those with extra storage of carbohydrate in the fruit (grain) for our own consumption. To do this we selected for excessive photosynthesis, temporary storage of excess carbohydrates in the pith of the stalk and eventual movement of it to the grain. This was not done cheaply. We had to get more leaf area and more root tissue to not only support the plants but also to uptake the water and nutrients to grow the bigger plant and to initiate the larger grains. All of this required more energy. After pollination, the newly formed embryo in each kernel begins to produce the cytokinins directing the flow of sugar towards it. This is occurring at the same time that root tips are not as prolific and consequently producing less cytokinin.
It takes about 10 days after pollination for the flow to each kernel to gain full speed. Varieties, and environments, differ in the flow rate per kernel but from day 11 to about day 40 the flow per kernel appears to be constant. Production of sugars per day may be affected by cloudy days, or leaf damage but the power of the individual kernel sinks remains strong during that time. Any shortage of new sugar is replaced by sugars stored in the stalk pith tissue. After the 50thday, the draw per day is reduced until finally an abscission layer is formed at the base of the kernel in which the phloem tissue no longer can move the sugars. However during that 60-day period the root is competing with the kernels for sugars and our attempt to capture the maximum carbohydrate in the grain.
Nutrition and moisture in corn silks allow the fast movement of the pollen tube towards the ovule and contribution of the male genetics to the next generation. Those same favorable silk characteristics also can be used by invading fungi. Rapid deterioration of the silk tissue after pollen tube growth offers protection within a few days after pollination, but environments and genetics can have a drastic effect on the time of silk vulnerability and the biology of potential invaders. Aspergillus flavusgets much attention because of is dangerous toxin produced on infected corn. Fusarium verticilloidesis another common invader of corn kernels through silk infection that can produce a mycotoxin (i.e. fumonisin). Others such as Diplodia maydisand Gibberella zeaealso can utilize the silks and initial entry into the ear.
These fungi are mostly saprophytic feeders on plant debris and intensity of their spore production is greatly dependent of corn debris from the previous season near the new crop plants. Their biology also is influenced by the environment affecting competition with other saprophytes feeding on debris and production of spores when the silks are exposed.
Duration of silk vulnerability is also associated with environment. Cool, moist weather a few weeks before normal pollination may cause silks to be exposed before pollen is produced- and may favor Diplodia(Stenocarpella) maydis. Extended dry, warm periods during the pre-pollination time, may cause pollen production before silk elongation and exposure but favor Aspergillus flavussporulation and distribution by the time the un-pollinated silks do emerge. Fusarium species (including Gibberella zeae) produce massive numbers of spores under most environments.
Plant pathologist have shown that one can induce ear infection by directly spraying the silks with the spores of each of these pathogens. These studies have shown evidence of resistance variance among genotypes but usually only on a scale and not of absolute absence of disease. Evaluation for resistance from natural infection is not easy. One can record occurrence of infection within plots, but each genotype may not be exposed to the same environments, including time of silk exposure. One does need to use care before drawing conclusions about ear rot susceptibility based upon single location observations.
Ear rots are prime examples of the complex biology of host and pathogens interacting with environments. Ear rot may not be noticed until harvest, but the problem involved the dynamics occurring at pollination time of the season.
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.