Corn’s unique biology and history contributes to the crop’s worldwide distribution and productivity today. About 8-10000 years ago, probably in the Balsas River valley of Mexico, someone or perhaps several people, found a mutant teosinte plant in which the hard fruit casing did not extend fully around the enclosed single seeded grain, the kernel. Someone realized that this made the kernel very edible and consequently propagated some of the seed. It was recently discovered that a single mutation in the TGA1 gene in Teosinte, changed a single nucleotide in the DNA code of this gene. This resulted in an amino acid change (asparagine instead of lysine) component of a protein critical to the development of the seed case in Teosinte and corn. Not only were the starch components of the seed more easily extracted by humans, but removal of the hard case allowed for greater growth of the kernels. This was only one of several mutations that ultimately resulted in we know as maize but we are appreciative that people a very long time ago, recognized the advantage of this mutation. A description of the mutation is in http://phys.org/news/2015-07-tiny-genetic-tweak-corn-kernels.html.
Other mutations assisted humans as they moved from a plant with about 20 seeds per ‘ear’ encased in a hard covering, into a plant that were easily used for food. It is notable that the initial mutation was to an annual plant version of Teosinte, thus allowing for selection of new genetics each year. A thousand years could equal 40-50 generations of humans but is 1000 generations of corn, allowing a lot of opportunity for genetic changes as humans made selections for adaptation to the environments and their food.
There is archeological data supporting that the early corn, although originating in a valley in south central Mexico, was moved to the highlands of Mexico.
The first European exposure to corn was about 500 years ago. Europeans called it corn because that was the common name for other grains. Seed was moved to Europe where it spread from even further to Africa and Asia, again with locals selecting for adaptation to their conditions. This included a wide range of required time from planting to harvest, disease pressure and local food uses.
Within the USA, corn that moved through the Southwest and then north and east tended to be flint types whereas the Southeast corn was floury types perhaps with genetics influenced by Caribbean corn migration. Flint corns in the Northeast USA tended to have fewer kernel rows than the semi-dent types of the southeast. As people became more stationary, with each farmer having the opportunity to saved seed that favored their environment, food and livestock needs, multiple uniquely genetic varieties developed across the continent. Although local selections were based upon gross performance, ultimately selections were having effects on root structures, photosynthesis parameters, moisture stress tolerance, germination in cool soils, and disease resistance. Separation of the male and female flowers of corn became a major asset to avoid complete inbreeding as farmers kept desirable ears to save for the next season. Most pollen from an individual corn plant does not fall on its own silk, almost guaranteeing cross pollination in open fields. Until 80 years ago, open pollinated varieties were the sources of corn, with yields in the USA usually less than 30 bushels per acre.
Those corn breeders contributed to the wide genetic diversity for current corn breeders to tap into for the latest traits needed for successful crops.
As the corn crop is being harvested in North America one can easily marvel how a tropical grass called teosinte that reseeded itself by easily detaching mature seed and allowing easy scattering for the next generation. One also has to marvel at the humans that recolonized the genetic potential, before we knew about genes, of this weedy plant with a few seed growing in central Mexico. The path to modern corn progressed by people some 8-10000 years ago by selecting the mutants that did not scatter the seed, that deposited larger amounts of carbohydrates in the kernel, and had other characteristics allowing for better harvests and human use as they gathered the seed.
People who traveled through those areas found they could carry this seed and later successfully found mutants that would adapt to new environments. This plant’s ease of cross fertilization provided more genetic diversity, and normal mutation rates, provided increasing diversity for many plant and kernel characteristics desired by each group of people as well as the carbohydrate nutrition needed for human health.
The genetic features that evolved previous to human effort probably included a photosynthesis mechanism that allows more efficient use of atmospheric CO2 and sunlight than most plant species. This C4 photosynthesis has an advantage over most plants’ C3 photosynthesis by continuing to increase production and storage of carbohydrates even with the brightest of sunlight.
Humans from the food-gathering folks to all of those today working with this crop learned to cultivate it in multiple environments including soils, nutrients and to manipulate and select genetics best meeting the needs of people. Corn has come a long way and it will continue as we learn more of the potential of Zea mays.
Resistance to stalk rot fungi involves so much of the corn plant’s biology and the environment that it does not become an easy trait to express in hybrid descriptions. On the other hand, there are differences in the tendencies to develop stalk rot when the plants are under certain environments. Hybrids differ in reaction to favorable pre-pollination conditions, some committing to greater movement of carbohydrates to the grain at the detriment of carbohydrate availability to the roots. Reactions to late season photosynthetic stress also varies among hybrids.
The gradations of these variables and hybrid reactions do not allow absolute stalk rot resistance ratings possible. Expression of stalk rot rating is much like expression of corn yield- absolute values are not appropriate but are only meaningful in relation to other hybrids or acceptable performance. It is in this regard that evaluation of stalk rot vulnerability of experimental hybrids by plant breeders needs to be done in hybrid yield tests. Stalk rot vulnerability is a hybrid phenomenon that may be influenced by the inbred parents, but it is mostly the product of heterosis, with the combination of the parent genetics affecting the probability of stalk rot problems. Consequently, it is evaluation of the hybrid that is critical. Also, just as with yield testing, commercial seed breeders are interested in predicting the stalk rot vulnerability in the field where the hybrid will be used.
Plot yields can be taken with accuracy, but evaluation of stalk rot requires human observation. Counting lodged plants is relatively easily done from the harvest combine but this method does not consider the rotted plants still standing but ready to lodge with the next strong wind. An alternative is to rate the stalk condition by walking each plot, giving it an acceptability rating. If all plants are strong and with green lower stalk color, the plot is scored as excellent. If too many plants are weak and ready to lodge, making it unacceptable, then it can be scored as extremely unacceptable. Of course, some plots would be scored as intermediate. This method should be applied at all plot locations. The final summary can be expressed as the percentage of plots or location in which a hybrid had acceptable levels of stalk rot. This should allow an estimation of the frequency of stalk rot problems expected for each hybrid. Test plot locations will not represent all the environments that a commercial hybrid will need to balance yield, stresses and stalk rot but growers will evaluate annually in their field conditions.
Stalk rot resistance ratings should not be considered as absolute resistance by hybrids against a specific late season fungus but more of the balance of photosynthetic stress and translocation of carbohydrates under most field conditions.
(Article from Corn Journal 10/19/2017)
There is a tendency to give the identity of the most obvious fungus in a rotting stalk as the cause when significant lodging occurs in a corn field. It is Diplodia, or Anthracnose or Fusarium or Gibberella because these are the most easily identified fungi on the rotting material. In fact, multiple other fungi are probably in the same stalk rotting the dead stalk tissue. Most importantly, these fungi did not cause the stalk tissue to die but entered after the stalk tissue died. Living corn tissue fends off these and the many other potential saprophytes in and on soil debris. Any of these fungi successfully invade the stalk tissue when the plant tissue no longer produces the metabolites to fend off these potential saprophytes.
When analyzing the cause of significant stalk rot in a field, one needs to look for the reason the plant lost its ability to fend off the fungus and lost its strength to stay upright. A third of that strength is due to the lower stalk tissue that has pith tissue connected to the outer rind cells, essentially forming a rod. These pith cells are large parenchyma cells filled with liquid and stored, soluble carbohydrates. These carbohydrates are available to the roots for their metabolism and, when called upon by the hormones directing flow, also to the newly forming kernels. If previous and continuing photosynthesis in the plant produces enough carbohydrate to meet the demand of the kernels and the roots the plant maintains succulent, living pith tissue throughout the stalk and thereby maintaining the stalk strength. Potential invaders are warded off by the metabolism of those living cells.
Discerning the cause of why one plant died and lodged and not all plants require a more diligent search than simply naming the most obvious fungus. Pith tissue died prematurely and shrunk away from the stalk rind, changing the structure from a solid rod to a hollow tube. Furthermore, those multiple saprophytes easily invaded the dead tissue, further weakening the stalk.
The analysis of why has to include reasons why was there not enough carbohydrate in the pith tissue of the rotted stalk to maintain living pith cells. It is not as simple as naming the dominant fungus in the dead stalk
Several aspects of the tar spot fungus, Phyllachora maydis. Appears to be unique corn leaf pathogens. It belongs to a group of fungi called Ascomycetes, because its sexual reproduction stage involves formation of an ascus after the fusion of two nuclei. Miosis occurs to produce 4 haploid single cells each of which divides to produce 8 ascospores within a sac called an ascus. A thick-walled group of cells form black ‘stromata’ on the surface of the leaf enclosing several of these spore-containing asci. With the right environment, such as a humid warm night, the spores are released from the ascus and easily moved in the wind. After germinating on the surface of the corn leaf, the hyphae establish specialized structure that grows into the leaf. Apparently, within susceptible hosts, the fungus absorbs nutrients and reproduces soon, again releasing spores into the air.
Many corn leaf pathogens are ascomycetes but most of the fungal spread is done be asexual reproduction, with conidia the pathogen spreading mechanism, with the sexual stage being restricted to end of season reproduction. Although genetic mutation can occur within the fungus before conidial reproduction, this opportunity for development of new genetic combinations is not as profound as with fusion followed by meiosis such as in meiosis following the sexual union of nuclei. This may allow variants to continually develop within this pathogen.
Being an obligate pathogen, only known to grow on living corn leaves, certainly makes study more difficult but eventually some of the variation will become understood. Currently no other host has been identified but genetic variability would make this a possibility. Widespread outbreaks like in summer of 2021 seemed to favor this disease. Perhaps variants will also adapt to less humid weather as well.
This disease has potential to cause significant damage to corn and must be studied with urgency.
Tar Spot of corn became an important problem in Northern USA corn belt states in 2021. It has drawn the attention of several corn pathologists that summarized their observations of the past few years in Oct. 2020 publication of Plant Disease Vol.104, No. 10. The main pathogen causing the disease is an obligate pathogen, meaning that it can not be cultured on artificial media. This characteristic hinders rapid investigations of the disease. Its spread appears to be related to temperatures and humidity, again making intense annual studies difficult because of inconsistent occurrence.
The spores of this fungus are easily spread in wind, apparently for several miles. Spores can overwinter in corn debris, infect corn pants at all stages and set up spread within and outside the field if humidity is relatively high for prolonged times. There appears to be no complete resistance among today’s corn hybrids but a range of susceptibility from those that seem to have few lesions to those that are completely killed before normal black layer. Uneven and somewhat unpredictable spread of the disease has complicated the evaluation of disease resistance. We at PSR attempted to rate hybrids for resistance among hybrids submitted by seed companies for evaluation of resistance to other diseases. In 2021, our nursery seemingly suddenly showed most plants with Tar Spot. The black spots on most leaves in many hybrids often interfering with other disease symptoms. Leaves appeared to die prematurely. Those with mostly green leaves were tentatively appearing as more resistant to tar spot with the potential that relative maturity was complexing the ratings. Checking those that had green leaves 7 days later, remained green, consistent with actual resistance and not maturity as the main factor in reaction to this disease.
This 2021 small nursery was isolated from other corn for at least a mile. We saw tar spot in the field 2 years ago but very little last year, supporting the hypothesis that this year’s infection was mostly from spores spread from some distance. Although our field has been in corn for several years, it had very little of last year’s debris before planting.
This disease was identified in corn in Mexico in 1905, but, I think, only identified in corn in the Midwest area in 2015. Hopefully more knowledge will be gained from the 2021 experience, and we will find more on how to protect corn. Corn genetics, weather, pathogens and agriculture are in constant change resulting in new disease occurrences.
Corn stalks have a green outer rind color during most of the growing season as the outer cells are pigmented by the chlorophyll. This color continues beyond grain fill as this annual plant matures without wilting, even up to normal grain harvest. If the plant wilts because of root rot, not only do the leaves desiccate, turning from a green color to gray within a few days and then brown but the stalk color changes also. The dark green color becomes yellow-green a few days after the plant wilt. This color change progresses to yellow and a few days later to brown.
As the brown color intensifies, desiccation of the internal pith causes withdrawal of the pith from the outer rind. This changes the stalk structure from a solid rod to a tube, reducing the strength by a third, leaving it vulnerable to breakage. One can access this vulnerability by gently pushing the stalks or pinching the lower stem. Visual inspection of the color of the lower stalks to judge this deterioration also can be used to evaluate the plant’s vulnerability to lodging. Individual plants with green lower stalks a few days after grain ‘black layer’ will remain intact through harvest.
The anthracnose fungus, Colletotrichum graminicola, will cause black streaks on the outer rind even on a green stalk. This color only intensifies, however, if the plant wilts, apparently because the living cells can restrict the fungus. If there remains a green color around the black streaks, the lodging threat is not great. Another interaction with the fungus commonly occurs in the uppermost internode of the corn plant. It is often noted that this internode turns brown when remaining stalk is green. As sugars are moved from leaves to the grain, this upper internode often is depleted first resulting in senescence of this tissue. The anthracnose fungus is often found in the dying tissue. I interpret it mostly as signal that the plant is successfully moving maximum carbs to grain and not necessarily a sign of stalk rot.
Other fungi also become noticeable on the dead, brown lower stalks. Gibberella zeae produces its reproductive bodies near the nodes, Diplodia maydis produces theirs more scattered on the internode tissue and Fusarium moniliforme gives a pinkish discoloration across the internode surface. It may give us some comfort to have a name for the fungus present but it must be remembered that the cause was insufficient carbohydrate to both meet the translocation demands of the grain and the maintenance of root life. These fungi, and the many others also digesting the senescing and dead stalk tissue were not actively killing the plant.
One must not forget that naming the fungus most obvious on the dead stalk is not the same as identifying the cause of the plant wilting early and the resulting weakening of the stalk tissue. Best to look further into the dynamics of all factors that kept the plant from finishing the season with green and solid lower stalk.
As the sugars in the corn plant move to developing kernels, each individual plant differs in number of kernels and supply of stored sugars as well as daily differences in photosynthesis. Shading of leaves by adjacent plants differs especially if distance between plants differs or if leaf pathogens differ. Water and mineral differences also could differ with soil differences. Although genetics may be the same, small environmental differences can affect total photosynthesis even between adjacent plants in a corn field.
Transportation of sugars to the ear is largely affected by number of ovules pollinated and genetics of the hybrid. After the first 10 days after pollination, there is a constant and consistent pull of sugars to the kernels. This is daily, regardless of daily variation of photosynthesis caused by cloudy and dark days. Sugars are transported from storage in stalk tissue if not available from leaves.
Sugars in the stalk are also used to supply energy for root cell metabolism. Root tissue started deteriorating shortly after pollination, but the speed of that deterioration is at least partly determined by sugar supplied from above ground sources. Metabolism of root cells is essential for resisting invasion by fungi in the soil. Plugging of the vascular system by these fungi interferes with the water intake from the soil and transport in the xylem to the stem and leaves.
Meanwhile, transpiration of water through leaf stomates continues at a rate determined by usual dynamics, hot dry days requiring more water transported from roots to keep the leaves turgid. Furthermore, water is the solvent for the sugars to be moved from the leaf cytoplasm to and in the phloem to the developing kernels.
Water in the stalk also contributes to the stalk strength, especially by keeping the pith cells swollen and adjacent to the outer rind cells, essentially keeping the stalk with the physical strength of a rod.
A lot of things are happening in each corn plant that we can’t see but each of these plants is essentially on its own, as dictated by its genetics and environment.
Stalk rot nearly always begins as a root rot. Root rot by organisms is nearly always occurs because the root suffers from lack of sugars supplied from above ground to parts of the plant. The symptom we see is plant wilting and lower stalk turning brown but the below the soil surface, the root is deteriorating.
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.
Below is from blogs that I wrote in 2015. The principles of factors involving stalkrot continues in fields today.
With a B.S. degree in Botany from Iowa State I was lucky to teach biology in Sarawak as a Peace Corps volunteer in 1963 and 1964. Probably like all teachers, I soon discovered how little I knew about my subjects. Among the many benefits of that job was the short term. It was assumed that one would leave, and for me that meant grad school and a chance to learn more about plants and fungi. After more studies in Botany and Mycology I took a job with a seed corn company in which studies of plants and fungi was forced to face the realities of corn grown in many environments and considered as a crop instead of individual plants. I was hired because of the corn industry concerns that their crop’s vulnerability to disease had been exposed with race T of southern corn leaf blight in 1970. I, nor the seed company, had real clear ideas of what a plant pathologist should do in a company breeding corn seed varieties. I had a lot to learn.
After southern corn leaf blight danger subsided, corn breeders advised me that their toughest problem was obtaining resistance to stalk rot. So I was a guy with an interest in biology of plants faced with a complex problem. Why does stalk rot occur in one plant but not the next? Single cross hybrid plants are, at least theoretically, genetically identical. The fungi accused of causing stalk rot are ubiquitous and surely readily available to attach each plant. So, why this plant and not the next?
A dead plant with yellow lower stalk is adjacent to a genetically identical plant with a green live lower stalk. Why? I first hypothesized these could be the plants that emerged late, as if it developed from seed that germinated slowly because of deteriorating quality. In the field nursery with many hybrids tags were put by plants that showed only 3 leaves and other tags placed by seedlings just emerging when most adjacent plants were showing 5 leaves. These plants were followed through the season. Late emerging plants definitely did not develop stalk rot. Some of those that were only emerging when tagged actually disappeared but if not they were completely barren. Those tagged with 3 leaves had narrow stalks and tassels that were much smaller and with fewer branches than surrounding plants, silks emerging later than other plants and averaged about 20% of the yield of majority plants- but no stalkrot. I showed the plants to the fellow that evaluated winter growouts for purity of new seed lots. He said that confirmed his opinion that some plants he saw that looked like they could be inbred selfs were actually late emerging plants. To make sure that these were not inbreds, the next year I hand planted 5 hybrids leaving interplant space for planting the same hybrids later between the initial planting. These intentional late emergence plants looked the same as in the first year’s observation. Late emergers apparently suffer from competition resulting in having very small stalks and yield but the stalks remain green. Late emerging plants do not yield but also do not explain why adjacent plants do not behave the same in terms of stalk rot.
The concept that late emerging plants do not perform well and that seed quality is a significant component to good grain yields was observed by many others before that experiment in 1973, but it was new to me. It also set me on path to find a better method of evaluating purity of hybrid seed lots as well as finding other explanations as to why a dead plant would occur adjacent to a green one only a few inches apart. It is probably significant that commercial hybrids of 2015 have a lot less ‘flex’ than those of 1973, but the basic importance of uniform emergence remains.
If a corn plant draws more carbohydrates to the ear during those critical 60 days after pollination than it can supply with current photosynthesis and storage in the stalk, it depletes the supply needed to keep root cell’s metabolism. The deterioration of root cell metabolism allows invasion of organisms in the soil and inability of the roots to transport water to the plant parts above the soil. Transpiration from the leaves continues until all available water is gone. Then the plant wilts. Symptoms of the wilt become slightly visible for a few days before all leaves turn gray and droop. We call this premature death. These wilted plants occur as individuals, often surrounded by green plants that did not overdraw on its carbohydrate supply to fill its kernels. Often these individual wilted plants have more kernels than those adjacent green plants or have excess photosynthetic stresses.
The wilted plants initially have green outer rind to the lower stalk, but the pith tissue inside the stalk has puled away from the outer rind, as part of the wilting process. This weakens the stalk strength by one third. The outer rind slowly turns from a green color to yellow and shows symptoms of invasion of fungi as they digest the remaining cellulose and proteins in the stalk cells, further weakening the stalk strength.
The critical stresses leading to stalk rot occur during the kernel fill period, those 60 days after pollination. If a plant makes it through that time without wilting, it probably will not get premature root ands stalk rot by normal harvest time. Inspection of corn plants about 60 days after pollination allows the grower to access the to predict probability of stalk rot and lodging in the field that season. Individual gray plants with yellow and brown color to outer rind of the lowest 2-3 above-ground nodes are most likely to lodge with slight wind pressure. These plants easily fall with slight pressure. One can also easily pull the plants up from the soil as the dead roots offer little resistance.
Why did that plant commit more to kernel fill that its photosynthesis could supply? Was it shaded by adjacent plants because of inadequate spacing of seed, did it have excess damage to leaves from pathogens or insects. Did the environment of the roots cause less root mass or destruction from pathogens or insects? Perhaps the genetics of the hybrid encouraged a higher kernel number in that environment than could be supported under the photosynthetic stress of the season.
Having a few early wilted plants in a field can be a sign that the hybrid maximized its ability to produce grain yield for that season’s environment. One can learn a lot with inspection of the field shortly after the 60-day kernel fill period.
Sugars are transported to each kernel for days 10-50 after pollination if most corn plants if field conditions are favorable. Then the transport slows for another 10 days.
Each kernel in a corn ear is a fruit. As with most other fruits, sugars are transported to the kernel through the vascular system from the leaves and the stem. Plant hormones like auxins and gibberellins produced in the seed embryo meristems actively guide the sugars to the seed within the fruit. Corn kernels have only one seed. Although much of the sugar is moved outside of the embryo to the endosperm, sugar also provides energy for growth and development of the embryo. As the embryo matures, auxin production is reduced. Consequently, physiological demand for sucrose supply to the kernel is reduced.
Reduction of sucrose in the cells at the base of the kernel causes the balance of ethylene and auxin to change. Ethylene increase causes the layer of parenchyma cells closest to the kernel base to lose cell wall contents, while those adjacent cells away from the kernel gain wall thickness. Eventually an abscission layer forms cutting off all movement of sugar into the kernel and water movement away from the kernel thru the stem tissue (the cob).
Research by J.J. Afuakwa, Crookston and R.J Jones (Crop. Sci. 24. 285-288) showed that reduction of sucrose available to the kernel was a major factor in induction of the abscission layer (black layer). Although it is mostly related to maturation of the embryo, it could be induced by other factors reducing sucrose supply to kernels. Reduction of photosynthesis by leaf disease or frost damaged leaves could result in shortened time to black layer. Early plant death, perhaps from root rot, causing leaves to wilt and thus removing sugar supplies induce black layer within a few days.
Plants with green leaves 60 days after pollination now will undergo slow maturation with abscission layers forming at the base of each leaf. Those abscission layers cut off the transport of sugars from the leaves and the transport of water to the leaves and removal of water from the plant via transpiration. Reduced competition with kernels for sugars stored in the stalk pith tissue allows roots to slowly age.
Plants that did not manage to make it the full 60 days with green leaves likely had photosynthetic stress reducing the ability to meet the demand by kernels for sugars. As a result, root tissue on that plant lost its ability to adequately battle the multiple potential pathogens. Loss of living root tissue during the kernel fill period results in less water uptake and consequently early wilting of the entire corn plant. Kernel filling stops at that time.
Competition for carbohydrates between kernels in developing ear and plant metabolism sites especially in the roots of a corn plant is established 10 days after pollination. This is a battle being fought individually by each plant in a corn field, as each plant can have slightly different environmental factors influencing its ability to produce carbohydrates and different numbers of kernels.
Net supply of carbs is influenced by environments, like light intensity, in which the rate of photosynthesis drops directly with less light. Cloudy days result in lass carbs produced. Leaf disease, reducing photosynthesis due to less leaf area, as does shade from adjacent plants. We have selected genetics programed to move carbs to non-photosynthesizing tissue like the roots with excess stored in stalk. During the grain fill time of the corn plant, newly produced carbs are transported to the kernels as well as those stored in the stalk pith tissue. The draw to kernels is constant, influenced by genetics and minerals, regardless of daily photosynthesis factors. Competition between kernel development and root cell metabolism for carbohydrates reserves stored in the stalk tissue becomes more intense if daily photosynthesis is reduced during the 40-day period of maximum draw by developing kernels.
Energy supplied by the carbohydrates pulled to the root tissue is used in its cells’ metabolism for normal function including producing the compounds needed to ward off the multiple organisms in the soil attempting to devour the root tissue. Defense of the living, functioning root tissue is essential to the rest of the corn plant, as the minerals and water absorbed by roots and transferred upwards are essential to function.
It is a battle essentially between roots and kernels for carbs that is fought by each individual plant in a corn plant especially between day 10 and day 50 after pollination. If carb supply is not sufficient to meet both needs, kernels win the race. The roots degenerate prematurely and are unable to supply the water to leaves to match the loss of leaf water due to transpiration. As a result, the plant wilts. Kernels’ win is temporary, as the wilted plant no longer can transport carbs to kernels.
Photosynthesis is the engine driving corn from the seedling to maturity. Previous generation's photosynthesis provided the energy for the seedling to emerge from the soil. Current generation photosynthesis provides more than sufficient energy for the metabolism to build tissue to construct a plant with expansive roots, large leaves, and 6-9 feet of stalk within a few months of seedling emergence. The corn plant not only provides the energy for the building materials for its new structures and daily metabolism but also has excess carbohydrates that are stored in the stalk pith cells.
Then, at midseason, it produces flowers. After pollination for the female flowers, hormones in the plant shifts the direction of flow of the carbohydrates from leaves and stalk pith cells to the the new embryos and its storage compartment, the endosperm. Environment and genetics determine the rate of flow of carbohydrates to the new fruit of the corn plant. The number of fruits (kernels) also becomes a big influence on the total draw from the carbohydrate supply.
Flow for first 10 days after pollination is relatively slow but then it speeds to a faster, relentless pace for the next 40 days. That daily pace of movement of carbs to the ear on the plant continues regardless of daily variation in photosynthetic rates due to environmental variables. If cloudy weather slows photosynthesis, the reserves in the stalk provide the difference. If leave disease reduces leaf area available to light energy conversion to carbohydrates, storage from early days is called upon for movement to the new kernels.
This high rate of flow of carbs to the new kernels slows after day 50 for about 10 days until it is cut off with the formation of an abscission layer at the base of each kernel. If the other plant parts such as the root tissue survived the competition for stored carbohydrates in the stalk, slow senescence occurs in the plant cells. This is the outcome desired by all corn growers but environmental stresses can interfere with the completion of maximum deposit of carbs in the kernel on living plants.
About 5-6 weeks after pollination is a good time to evaluate corn hybrids for resistance to leaf disease. This Corn Journal blog from 2017 discusses some of the dynamics in resistance to leaf diseases.
Leaf epidermal cell’s walls and the waxy leaf surface provide the first line of defense against microbes. Pathogens adapted to overcoming this defense set off the next defense system after penetrating the leaf. This is initiated by the plant detecting the presence of the intruder. Plant cells nearby detect the presence of a protein exuded by the pathogen. Such proteins are called effectors, as they are detected chemically by host cells near the invader. Upon detection, these adjacent host cells produce potential microbe-inhibiting compounds such as reactive oxygen, nitric oxide, specific enzymes, salicylic acid and other hormones to effectively thwart the pathogen growth. Much initial reaction is limited to host cells adjacent to the infection site.
Resistance to corn leaf pathogens such as Exserohilum turcicum, cause of northern leaf blight, Cercospora zeae-maydis (gray leaf spot) and Bipolaris maydis (southern corn leaf blight)
Involve detection of that specific pathogen and production of more general antimicrobial products in the immediate area of the pathogen. These two steps are inherited independently. Perhaps the pathogen detection system is more specific to the pathogen, accounting for a corn variety being more resistant to one pathogen than another. On the other hand, I am suspicious that if two pathogens arrive in the same area of the plant, only one will survive, as if the plant reacts to the first one by producing general resistance compound that inhibit the infection by the second one to arrive in the same area.
The system described above is referred to as general or horizontal resistance. It is controlled by 3-5 genes for products to detect and reduce spread of the pathogen. Horizontal resistance is expressed in corn plants by fewer leaf disease lesions. Evaluation of varieties for this type of lesion has some ambiguity however, because the number of lesions or amount of leaf damage is also affected by the intensity of disease pressure. Heavily diseased leaves from the previous season in fields of low tillage, with frequent early season rain can result in more leaf lesions in a variety of good general resistance to a pathogen than will occur in one of poor resistance with little disease pressure.
Every growing season, every field, every hybrid has some difference in dynamics affecting corn leaf diseases. The primary process, however, remains the same. Fertilization of the of the embryos in the ear induces physiological changes in the leaves as movement of carbohydrates emphasizes the developing kernels.
Annual plants such as maize are genetically programmed to salvage nutrients from leaves after pollination, resulting in senescence of the leaves. One study (http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0115617) maintained that it begins in the ear leaf of corn as early as 14 days after pollination. These authors found at least 4500 genes involved in the biosynthesis of the senescence process as degradation of leaf cell components and new proteins were made, resulting in the regulated movement of nutrients and sugars from the leaf to the developing ear.
This phenomenon is not unlike the reabsorption of leaf nutrients that occurs in many plants species and is being expressed in the Northern Hemisphere currently in deciduous trees, as the senescing leaves lose nutrients and chlorophyll, eventually abscising from the branch. The similar process in corn begins with the degradation and removal of leaf cellular contents, transportation to the fruit (grain) and eventual development of thickened cells at the base of the leaf, cutting off all movement of water and nutrients in and out of the leaf.
Varieties of corn surely differ in the timing and effectiveness of this senescence process. These differences may be reflected in leaf cellular activity such as leaf disease resistance or drought stress. The modified leaves composing the ear husk undergo the same senescing process, eventually effecting the opening of the husk needed for the evaporative drying of pre-harvest grain. Eventually, the senescing leaves are cut off from the rest of the plant by the development of thick walls in the parenchyma cells at the base of the leaf, similar to the abscission layer known as the black layer at the base of a mature kernel. The cutting off of the water into the leaf after the abscission layer is evidenced by the sagging of the leaf.
Leaf disease in a particular field may be different than last season but will be similar in some other field but the dynamics will remain.
The move from a wild weed Teosinte to a productive grain crop that we know as corn was the result of humans observing and selecting plants in the field that best fit the desires of the grower. The breadth of genetics available was largely due to the separation of male and female flowers on the corn plant, encouraging cross pollination, and humans’ movement of the species to many environments modern corn has nearly 40000 genes located on its 10 pairs of chromosomes.
Corn has attracted the interest of plant scientists with many specialties such as plant pathology, entomology and cellular biology. Some biologists were interested in trying to isolate corn cells from the plant into cultures of the cells that could be replicated, experimented with and then finally manipulated to produce normal plants. Techniques were discovered with some plant species in the 1950’s but some species including corn were difficult to go from cultured cells to mature plant. In the early 1970’s, the combination the right mix of plant hormones and corn varieties, allowed the stimulation of cultured corn cells to produce mature plants. This opened the way for manipulating corn cells in culture to produce unique plant characteristics.
Entomologists, and growers, were finding the more intense cropping of corn was allowing insects to damage the crop. Among those was the corn borer, a moth that produced larvae caterpillars capable of entering the corn stalk and ultimately causing the stalk to break, making the machine harvest difficult. A similar insect causes damage to other plants such as tomatoes. People had discovered that spraying a culture of a bacterium called Bacillus thuringiensis on tomato plants killed the caterpillars on tomatoes. This bacterium from the soil had genes that produced a protein that disrupted the gut of the insect larvae.
Geneticists were able to isolate the gene in this bacterium, giving the label of BT, and set off on the task of getting the gene into corn cells. Eventually a modified gun was used to fire a pure culture of the BT gene into a corn cell culture, inserted the gene into the corn chromosome. After screening in labs for the insertion in right position in a chromosome, the cell produced the protein toxic to the corn borer insect. Stimulation of that cell to grow into mature plants allowed it to be crossed to more agronomically productive corn varieties.
Combinations of scientists with varied specialties, commercial and public, and corn growers has allowed the current use of genes transferred from other species into corn. Probably genes were exchanged between species in the evolution of all living forms over time, but humans have found ways to accelerate and manipulate this for their use.
I have been thinking (I Know, that is dangerous!) about the long history of corn and all the generations of people that have participated in corn as we know it today. A lot of what we see today, adaptation of this species to all continents on our planet as well as individual field environments is due to its unique biology and interactions with growers researcher.
About 10000 years ago, someone or maybe several people came upon a mutant in a variety of Teosinte in which the seed (kernel) was larger than most Teosinte seed. Probably already using this species for food, grinding the seed into a flour. This mutant must have been attractive and worth propagating. Further enhancement was encouraged by the fact that this and surrounding plants had sufficient distance from male and female parts that cross fertilization was common, allowing further mixing of genes. Selection by those people in Southern Mexico continued to select plants with a combination of genes that had bigger and more kernels, as well as other plant features to support the kernels. Furthermore, these kernels could easily be transported by people passing through and carried further south and north, the genetic breadth and mutations allowing eventual selection of varieties adapted to the northern order of USA, through the tropics of South America to its most temperate environments.
When first European discovered the Americas, they found that native tribes had this plant species as a food crop. As each tribe had multiple years of maintaining and selections among genetic variants, there was already a large genetic pool that would eventually allow the adaptation to other continents.
Today’s growers are doing the same thing, selecting the corn hybrid that most fits their environment and the seed producers have the incentive to respond by searching for the genetic combinations best matching these environments. The broad genetic base of about 40000 genes spread across the corn’s 10 chromosomes allows for continual selection of the best fit.
Corn characteristics of its photosynthesis utilization of highest light intensity, separation of male and female flowers, annual maturity, efficient movement of carbohydrates to kernels supported with a broad genetic base has allowed this crop to become an international source of nutrition for humans.
Summer of 2021 features more rain variability in USA corn growing areas than usual. Leaf diseases such as northern leaf blight are greatly affected by the weather and consequently, so is the corn crop.
The disease is caused by the fungus Exserohilum turcicum (Setosphaeria turcica). The fungus lives in infected, dead or live leaves. It asexually produces spores (conidia) when the diseased tissue is moist and temperatures are proper for corn growth. The conidia have 4-6 cells arranged in a row and are light enough to be distributed by air currents within a corn field. After landing on a corn leaf, with a little moisture, in 3-6 hours the cells on both end of the conidia, begin dividing, emerging as germination tubes. These new hyphae quickly form a base on the surface called an appresorium, from which the fungus grows into the leaf epidermis. Within 12-18 hours after the conidia have landed on the leaf, it has successfully penetrated the leaf. There appears to be no difference in time to leaf penetration between the susceptible and resistant corn hybrids.
Chloroplasts near the infection point soon lose pigments as nearly 100 cells die, perhaps because of enzymatic activity of the fungus. This can be observed when small (0.5-1cm) circular, yellow spots show in the leaves in 24-48 hours after infection. From this initial location, the hyphae grow between cells towards the vascular bundles. Penetration of the vascular bundles is followed by plugging the xylem causing further death of surrounding cells dependent upon the water supplied through these tubes.
Resistance systems appear to begin after initial infection and perhaps mostly once the fungus has reached the vascular system. There does seem to be differences in that initial yellow spot in a couple days after infection and I wonder if the brighter color is not associated with greater quantitative resistance. Could part of quantitative resistance be self-destruction of cells near the infection point, depriving the fungus of nutrition? It does seem that initial spot is less obvious and possibly smaller in the more susceptible corn genotypes.
The wilted areas surrounding the plugged xylems eventually are depleted of living host cells. The fungus responds by producing new conidia within 14 days of the initial infection, ready to spread to more live leaves. Exserohilum turcicum remains viable in dry leaves for a number of years in dry environment, ready to produce conidia within 24 hours after moistened. Tillage, crop rotation and hybrid resistance become major factors in crop damage from this disease.
Annual plants such as corn, change physiology within a few months of the growing season. Corn has been bred to rapidly move maximum carbohydrates to the developing kernels. This has a profound affect on leaf disease resistance.
A few weeks after pollination, dynamics affecting resistance to leaf pathogens changes. Cytokinins are increasingly concentrated in the developing grain embryos, causing more translocation of sugars from leaf tissue to the ear, reducing availability for cellular metabolism in the leaf tissue. Leaves lower in the canopy, in the shadow of upper leaves have reduced photosynthetic rates due to receiving less than 5% of the light intensity as those exposed to full sunlight. Not having sufficient energy to maintain its cells, senescence of these leaves begins. Among those cell functions is the production of anti-pathogen biochemical that limit leaf pathogens.
Disease pressure increases in lower leaves with the higher humidity and longer dew periods that favor leaf pathogens. Cool, cloudy and wet weather in those 50 days of grain fill after pollination further favors the fungal leaf pathogens. This increased disease pressure on as leaf tissues occurs at the time in which they are losing the ability to react to invading organisms. Lowest leaves senesce first as the lower photosynthetic rate and increased disease kills tissue. Even weak pathogens, such as Fusariumspecies, invade the vascular tissue of such leaves causing the leaf to wilt, while the upper canopy leaves remain green and fully functional.
The senescence pattern progresses up the plant as it gets closer to meeting the active translocation period of 50 days after pollination. If there was exposure to pathogens such as Exserohilum turcicum, the cause of northern corn leaf blight, earlier in the season, the disease appears to move up the plant. This can cause difficulty in comparing resistance levels among hybrids varying in maturity such as in research plots. Those with earlier pollination dates may appear to be more susceptible, especially if the environment favored the disease, simply because the leaf senescence was more advanced than the later hybrids. This can be misleading not only in determining differences in innate resistance levels but also in predicting potential grain yield or increased stalk damage from the disease.
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.