Corn seedlings face soil environments with multiple potential pathogens and saprophytes. If stressed by cold wet weather that favor pathogens such as Pythium species, stimulated to grow towards seedlings leaking metabolites. If warmer, Fusarium species likewise are attracted to the living plant tissue. Resistance mechanism in the seedlings includes structures of the plant tissues and production of anti-fungal metabolites produced in the root and hypocotyl cells. The latter is influenced by heat energy, cell vitality and seedling ‘vigor’.
If an individual plant survives these early potential problems to emerge with 2-3 leaves, as nodal roots take over and the hypocotyl and earlier roots decline, the plant will usually not show the early wilt symptoms. Fusarium may have successfully penetrated earlier and make its way to the apical meristem without causing direct damage. It has been shown that even if the Fusarium hyphae were in the seed before planting, it does little visible damage until perhaps making its way to the new kernels by harvest.
When seedlings wilt in the field, it is difficult to assign a single cause. It is usually seen scattered among undamaged seedlings. Was it biological vigor or quality of that individual seed, microenvironment of that individual seed or scattered presence of a pathogen. Samples of dead seedlings will frequently show presence of Fusarium species but was it a cause of the seedling death or simply a quick invader of weakened plant tissue? This is not an easy problem to correctly analyze.
The first critical state of establishing a corn crop is with germination. This first stage allows the embryo radical to emerge and push downwards, establishing the primary root tissue, and the shoot tissue pushing upwards with the hypocotyl pushing the shoot meristem towards the light. As the hypocotyl grows, roots grow at its base and become temporary roots called seminal roots. Energy for these growths are dependent upon stored carbohydrates in the endosperm and conversion into usable energy in cells via mitochondria. Heat energy from the environment assists with these physiological moves. After the hypocotyl pushes the meristem to the light, the first leaves emerge and begin photosynthesis and resulting new carbohydrates for more growth. This extra energy allows the formation of secondary roots to begin at the nodes at the base of the shoot meristem, establishing the primary long-term nodal roots. These nodes remain under the soil surface. As more leaves form, and the lower higher nodes form above the soil surface these roots gain the dual function of absorbing and transporting water and minerals and supporting the stem. We often refer to these as brace roots.
Bob Nelson at Purdue has an informative summary of these root events (https://www.agry.purdue.edu/ext/corn/news/timeless/Roots.html)
If seed and environment cooperate, this next stage gets the corn crop off to a great start.
Speed and consistency of seedling emergence is the first observation of the spring season. We often use the term vigor to describe this phenomenon. Hybrids, lots and seed sizes will vary in ‘vigor’ but also environments. Usually it is not easy to clarify which of these factors were major. Hybrid vigor can be affected by genetics. In some cases, it is affected by which of two parent inbreds was used as seed parent because the female parent contributes the mitochondria, and their genetics, to the cells and thus the major source of converting the stored carbohydrates into the metabolic energy needed for cellular division and enlargement. Total genetics of hybrids also has an effect on growth speed.
Seed lots of identical hybrids can vary in seedling vigor. Stresses in seed field when the seed was produced can influence some seed to have poorer germination and early growth. It could be as simple as rain delaying timely harvest that allows metabolism in the embryo to continue whereas earlier harvest and drying would prevent this process. Storage at less than optimum temperatures and humidity can also allow aging to occur in some lots.
Field conditions with uneven consistency of soil components and surface debris also will affect uniformity of emergence. Too wet or too dry also varies.
Each spring brings its own field stress and challenges. There is no reason to think this year will be different.
Those first few weeks in the spring when the corn seed germinates and emerges can cause grower anxiety as the hypocotyl pushes upwards. Multiple species of fungi surround the tissue, attempting to enter the fresh growth. Interactions between seed physiological ‘vigor’, infection by fungi such as Fusarium species, environmental pressures including potential damaging organisms and seed treatments are complex.
A low percentage of seed within a seed bag are either dead of having sufficient cellular damage that all embryo cells do not function, perhaps with elongation of seminal root cells but no growth in the mesocotyl cells. Cell membranes damaged during seed maturation or with imbibition can self-repair, but this may result in delay of mesocotyl growth, delaying emergence compared to other seedlings and allowing more time for potential invasion by soil inhabiting fungi. Leakage of nutrients from the seed may also attract the fungi towards the germinating seed.
Fusarium species in the seed are not the only potential pathogens but also others are in nearly all soils. Fusarium verticilloides is one that tends to invade corn tissue after germination, perhaps growing between cells as the seedling extends beyond the soil surface. A few, such as F. graminearum often occupy the shoot base (crown), but it is not always clear if they significantly damage the plant. There is some evidence that presence of fungi in the emerging seedling correlates with reduced photosynthetic rate in leaves of the young plant.
Corn germinates and emerges more uniformly and quicker at 25°C (77°F) but temperate zone growers want to take advantage of the longer growing season by planting when soil temperature are only above 10-15°C. If the temperature remains low after planting, imbibitional damage to membranes is slow to repair and overall physiologic processes are slowed. Although Fusarium species are not favored by the low temperatures, the damaged tissue exudes nutrients to attract the fungi towards the tissue. Low temperatures also slow the production of resistance factors, allowing increased invasion of the tissue. This applies to the nodal roots that emerge after the seedling emerges as well. Soil components also affect the duration of exposure of mesocotyl if it has trouble pushing through the soil surface.
Seed treatments are intended to prevent or inhibit damage from seed-borne fungi and those potential pathogens infecting initial germinating seed. Polymers either added to the chemical fungicide treatments or even if used independent of the treatments can be helpful by slowing down the imbibitional process, potentially reducing the cell membrane damage. Most commercial seed treatments include a mix chemicals aimed at inhibiting fungi within the seed and a few components become somewhat systemic in the young seedlings. Application of seed treatments does require some care to make sure the seed does not absorb too much water and thus overcome the dormancy initiated by drying the seed. An interesting summary of Fusarium control by seed treatments can be found in a thesis at https://lib.dr.iastate.edu/rtd/15394
Among the human accomplishments of developing corn from a tropical grass (Teosinte) to extreme temperate zone environments has been the ability to get successful growth under less than perfect environments. This occurred with efforts of breeders selecting genetics, seed producers developing methods and growers working environments.
Elongation of seed embryo radical becoming the primary root system is often the first to emerge from the seed. Geotropism causes it to turn downwards. Shoot portion of the embryo emerges with a hypocotyl with a shoot meristem at its tip. Its direction of growth upwards is also part of the geotropism phenomenon. The timing of the growth in each direction is affected by heat energy and efficiency of the metabolism in the embryo cells. That energy is stored in the endosperm and translated into metabolic energy by the cell mitochondria. Deterioration of the cells through aging, moisture imbibition and physical damage to the corn embryo can affect the efficiency of these initial growths from the seed. Warmer temperature can minimize the damage by increasing the repair of damaged membranes in the cells.
Primary root growth has limited life as the seed source of energy is depleted. Hypocotyl upwards push towards soil surface until it detects far red light close to the soil surface. The final emergence coincides with emergence of the first collared leaf. This followed by a series of leaves. These leaves provide the energy not only for development of new green tissue but also the energy for new secondary roots growing from the first node of the stem at the base of the shoot in the soil. At this time the energy from the seed endosperm is no longer utilized as the primary root deteriorates.
The process for successful shoot emergence is dependent upon seed quality factors including genetics, especially of the female parent as the main supplier of mitochondria genetics, seed damage, field conditions including temperature.
It is amazing that the complex process is usually successful.
Corn seedlings are frequently attacked by a fungal-like organism of the Pythium genus when the soil is extremely cool and wet. Pythium belongs in a group of organisms called Oomycetes. These were once considered fungi, but more recent research has shown that they are more related to algae. Other pathogenic oomycetes include those causing diseases such as downy mildew of several grasses (including crazy top of corn) and Phytopthora root rot of many crops. Oomycetes were considered fungi because they usually produce filaments and spores plus they absorb nutrients from plants and animals. They differ from fungi by mostly lacking individual cells within the filaments, resulting in many nuclei within the long filaments. Most fungal cell walls are composed of chitin whereas the oomycete filament walls are cellulose, a difference that relates to the host resistance system. Often the first signal of fungal invasion is of the chitin, triggering the production of defense systems. Detection of an oomycete invasion requires a difference in plant chemistry.
Oomycetes frequently produce swimming spores that are released from overwintering spores (oospores) in the soil. Pythium spores, with flagella, swim to host root cells on which they grow hyphae to invade the host. Consequently, they cause the biggest problems in fields that are temporarily flooded with heavy rains and cool conditions. Studies have shown that 55°F is optimum for most Pythium species infecting corn in Midwest USA. The low temps probably slow down the host plant’s growth rate and inhibit potential competition from soil fungi.
As many as 18 species of Pythium have been shown to be pathogenic on corn. Often, they destroy the outer layer of the new root tissue. If this occurs before secondary roots become the main source of water uptake, the seedling will wilt. Although seed treatments can offer some protection, genetic diversity within a species often includes resistance to most treatment chemicals. Pythium genetic diversity also includes ability to attack rotation crops such as soybeans. Pythium species are easily isolated from soil but completely accounting for all the species or diverse genetics in regard to effective seed treatments or genetic resistance is not easy.
Control of the disease is best done with controlling water holding capacity of the soil.
Corn Journal Blog 03/22/2018
The Ht1 gene for resistance to the fungus causing northern leaf blight, Exserohilum turcicum, was effective during the 1970’s. This was before new races of the fungus that overcame the single resistance gene. One could detect the presence of the gene by putting the fungus on greenhouse-grown seedlings and evaluating for the distinctive resistance lesion that developed in about 10 days. As more inbreds, hybrids and segregating breeding materials were evaluated, it became clear that each corn genotype had distinct leaf morphological characters expressed in these young seedlings. Inbreds that had been deemed as pure from years of self-pollination had exactly identical expression of these characters, but segregating materials showed lack of uniformity in seedling morphology.
Previous experience with observations of late emerging plants that eventually resulting into deformed mature plants due to competition with adjacent corn plants led to the conclusion that one could evaluate for seed purity by observing seedlings closely in controlled greenhouse conditions. This led to a series of experiments and observations and eventual understanding that close observations of seedlings for certain key morphological features would allow evaluating genetic purity of hybrid and inbred seed lots. This technology has been applied by Professional Seed Research Inc. (PSR) since 1988 to multiple temperate and tropical hybrids for evaluation of purity (Seedling Growout®). Each corn genotype is distinct with seedling leaf morphology.
Close observation of seedling morphology also is implemented in corn breeding. As a trait is being crossed into an inbred, the segregates are formed with each generation of crosses, plants expressing the trait and having the most characteristics of the original parent can be selected for the next cross. Because the method allows observation of a large number of plants in a small space, this method can cut the number of generations needed to recover the desired inbred with the trait. PSR calls this corn backcrossing service Phenotype Select™.
Strange and fascinating how curiosity of those late emerging plants in the field and observations of seedlings could lead to new technology. Variables in crop-growing has provided many opportunities for participants to develop machinery and specific methodology for improving crop production.
I was pursuing an explanation of why did some plants wilt and develop stalk rot when adjacent plants stayed green and complete grain fill on solid stalks. Were these plants individuals that were stressed for the whole season because they emerged late? Why these individual plants? In the early 70’s we had a cold wet spring in the corn hybrid observation plot, with uneven seedling emergence and an opportunity to tag those individual plants that adjacent to earlier emerging plants. Those individual plants were observed during the season. They were obviously less ‘vigorous’ than adjacent plants, had narrow stalks, and delayed ear shoots. I asked the seedstock manager to look at these tagged plants to see if they looked like inbreds, created by selfing in the hybrid seed production field. He replied that he had seen similar plants before and said it does make evaluation of hybrid purity in winter ‘grow outs’ difficult. Final notes at the end of that season showed that these late emerging plants had significantly fewer kernels, if any at all.
These plants did not develop stalk rot. Were they impurities in the seed lot, perhaps inbreds? The following year, hybrid seed was hand planted with extra space between plants. When these seedlings emerged, the same hybrid seed was planted between the seedlings. Those late planted seedlings were observed during the season. As suspected, Late-emerging hybrid plants performed as those in the previous year, having spindly stalks and few kernels but no stalk rot.
Those observations led this young observer of corn to look at other possible explanations for why stalk rot of corn and more experiments and eventual conclusion that the individual stalk rot plants had produced more grain yield than those individual plants environment could support, essentially depriving the roots of needed photosynthesis products to keep them alive.
Late emerging plants were detracting from yield and not the ones that develop stalk rot.
At this time of the year in northern temperate zones, as growers are waiting for soil temperatures to be high enough for planting, one can contemplate why, no matter the position of the seed, does the root go down and the shoot go up. This has been studied by many, including Charles Darwin in 1880. The total mechanism is still not completely understood.
Geotropism is the response to gravity and phototropism is response to light. Root’s downward growth is affected by the tissue in the root tip meristem area. The root cap cells (outside the meristematic cells) effect the tropism. Removal of the cap appears to disorient the growth direction. Removal of cells on one side of the cap, causes the root to grow towards the remaining cells. It is possible that inner cell structures such as the endoplasmic reticulum, and other cell organelles tends to become more concentrated on the lower side of the cells and thus produces metabolites on that side, resulting in cell growth in that direction.
Plant hormones such as auxins and gibberellic acid are involved in plant tropism, but all of the exact mechanisms are still not understood. It has been proposed that auxins produced in the root tip are distributed to cells behind the root tip, affecting the elongation of exterior cells and thus direction of growth. Differences among corn varieties in root growth direction tendencies, some with more deep, narrow growth and others with more lateral growth, is evidence that genetic factors are influencing metabolism that affects root growth direction.
Phototropism is also affected by plant hormone production and distribution. Specific wave lengths in natural sunlight affect the auxins involved in the differential cell elongations, ultimately resulting in growth direction towards the light source. Exact mechanisms involving photo receptor compounds that allow specific wave lengths of light to turn on the growth cells is not clear, despite many researcher’s attempts to study specifics.
Tropism in plants is obvious and complex. Surely some of those 30,000-40,000 genes in corn are involved, and mostly we can only screen for the effects of the phenomenon with selecting the best performing corn plants and admire the fact that tropism exists.
(Corn Journal 4/19/2018)
Corn genetics and planting rates have changed a lot in the last 50 years. Breeding and selection of hybrids when planted in the USA Midwest at 22000 plants per acre required different genetics than when planted at 36000 plants per acre. Plants had more kernels supplied by more photosynthesis per plant. Higher densities with those hybrids would certainly develop the photosynthetic stress dynamics resulting in stalk rot because of insufficient carbs to supply both the grain and roots. More plants per acre, and slightly smaller ears per plant allowed a total of more grain, compensating for the reduction in photosynthesis per plant. On the other hand, these types of hybrids are more reliant on getting maximum number of productive plants. This is not only the necessity of high number of germinating seed but also that the seedling emerge uniformly. This was discussed in Corn Journal on 3/10/2016.
40 years ago, when pursuing the question of why one plant died early with stalk rot and the adjacent plant did not, I hypothesized that the dead plant was that one emerged late as a seedling. When most of the plants in the test plots showed their 5th leaf, a tag was put near those that had only 3 leaves and another marking those with only a spike. Notes were taken of these plants and their adjacent plant during the season. At pollination, it was clear that even those tagged at three leaves were not silking in time with adjacent plants and tended to have more slender stalks. Many of those tagged as spiking no longer were present, but those that survived were far off in pollination timing, had very small, narrow stalks and, eventually, small tassels. Ears were harvested at end of season and kernel numbers were counted. Those tagged with three leaves had only 20% of kernels of adjacent plants and those tagged as spike only were barren. Delayed emerging plants did not develop stalk rot but clearly the delay affected yield.
To eliminate the possibility that these delayed plants were not ‘selfed’ inbreds instead of hybrid plants, an experiment was performed the next season to confirm that emergence delay was the main factor. Seed was planted with twice the normal plant-to-plant spacing. When those seedlings spiked, the same hybrid seed was planted between the seedlings. This would be an unusual delay, but the effect was the same as the first observation. Barren plants, skinny stalks, small tassels were characteristic of the delayed emergence. Apparently, plant competition for late emerging plants has a drastic affect.
Others have done similar experiments before and after these done by a young guy beginning to learn about corn. My conclusion was that individual plants developing stalk rot were not the late emerging ones and that uniform emergence was an important factor in corn yields. Also, it was interesting that those late emergers could be confused with selfs, as confirmed by the fellow who normally evaluated hybrid purity in winter growouts. That eventually led to developing a different purity test method.
My experiments were done in the 70’s with hybrids and plant densities common at that time. It would be useful if similar experiments were done with more recent hybrids selected for consistent ear development at the higher plant densities used today. It is notable that experiments done by others have shown that among germination test methods, the cold test is the best predictor of field emergence and that it accounts for about 70% of differences among seed lots in field emergence.
Corn seed germination quality is always temporary. Female seed parent genetics, especially that of the mitochondria, area factor. Seed with dormancy because of low moisture content remains alive as long as the mitochondria have a low level of respiration to maintain membrane integrity, it becomes more difficult if kept in humid environments at temperatures greater than 50°F. We have seen many examples of seed kept on farms because 2019 weather prevented planting. Some will show in the field this spring.
Perhaps, for the first 8 centuries of corn culture, the percent of seedlings emerging from seed planted was not as significant as the amount and type of grain produced. Planting in hills or even by planters at low densities, favored genetics that produced larger ears if adjacent seed did not germinate. Modern terminology attempts to identify hybrids that adjust of lower density by producing larger ears defining them as ‘flex’ ear types. It is doubtful that there are only two types, flex and non-flex, but hybrids do have different tendencies when plants are less dense. There are hybrids that will tend to go barren if planted too dense and there are others that will only show competitive yields if planted at high densities. There are some that do not cut back on kernel numbers if crowded but will develop high percentage of stalk rot if planted too thick. Recent years of corn culture in the USA has led to hybrids that tolerate planting a 33% higher density than 40 years ago- and give more stable high yields than hybrids of that era.
These modern hybrids may have genetics for more photosynthesis per acre, at least due to increased leaf area, but also consistent silking when under the stress from competing plants. This may also favor selection of hybrids with less ‘flex’ and consequently a need for higher plant density. Although best knowledge of the ideal plant density in any season only becomes apparent after harvest, there is more pressure now than 40 years ago to have a uniform emergence percentage of 90+% every season.
Every seed within a single cross hybrid may be nearly genetically identical, but not with identical germination quality and not planted in identical microenvironments. Highest quality seed will tend to emerge uniformly, and seed producers make large efforts to produce such seed. However, even with best genetics, timely seed harvest and care in handling the seed it is rare that field emergence is perfect. It is a challenge to produce all seed lots with great quality and for testing systems to correctly predict the field emergence the following spring.
Corn seed dried properly to less than 15% moisture allows the mitochondria in the embryo cells to remain intact. Respiration in these mitochondria continues at a very slow rate, releasing sufficient energy to maintain membrane integrity of cell organelles. Genetics, especially of the female parent that supplied the mitochondria from its egg, affected this success as well as the physical conditions during seed development and harvest. Success gets revealed when the seed is planted. That process was described in Corn Journal blog 4/25/2017.
Very soon after the corn seed is planted, imbibition begins. The H2O activates the membrane-bound mitochondria to respire, providing energy for protein production. The enzymatic proteins include those that digest the starch stored in the endosperm into more sugar molecules to be transported through the scutellum to other cells in the embryo, resulting in more energy available to produce structures for cell elongation. Heat energy provides a regulatory function affecting the speed of this germination process. Imbibition occurs at any temperature but metabolic activity in corn is generally thought to be very low if seed environment is below 50°F. Speed of germination increases as the temperature increases.
Membrane integrity within the seed also affects the net speed of this process. Those individual seed with more damage are slower to sufficiently activate the system and thus slower to activate the metabolism needed for cell elongation in root (radicle) and the shoot sections of the embryo. Cool environments, delaying membrane repair, may result in death of the imbibed seed before the shoot can emerge from the soil. Some of these seed, even after warmed manage only to extend the root through the outer wall for the kernel, the shoot never emerging. Other weakened seed may finally get enough momentum to push through the soil surface but days after the healthier seed have emerged, resulting in a season-long competitive disadvantage. Heat energy during germination affects the severity of the effect of membrane damaged seed.
Microbes in the soil are generally warded off by products of seed metabolism in healthy seed. Those individual seeds that are slow to generate sufficient energy for growth are also more easily attacked by microbes, further slowing the germination process. Seed treatments are useful in giving the damaged seed more time to successfully germinate. Healthy seeds can successfully produce normal seedlings despite surrounding common soil microbes but those weaker individuals need the extra protection.
Imbibition is the movement of water through a membrane. This occurs in a corn seed when placed in a moist environment.
Corn seed, dead or alive, will allow water to enter through the pericarp, causing the kernel to swell. Dry cells in the embryo retain many membrane-bound structures including mitochondria, plastids including chloroplasts, nucleus and endoplasmic reticulum. Cellular membranes are composed of phospholipids and proteins organized in a manner that regulates the biological function of the cell organelles including regulation of movement of products in and out of the organelle.
Membranes in a dry corn seed cell are only slightly active, oxygen to pass through, for example but have more of a gel like structure. Within a few hours of imbibition, the structure changes as the phospholipids become moist and swollen. Resulting metabolism with activation of respiration in mitochondria, fueling gene translation in the nucleus, movement of RNA on the endoplasmic reticulum and production of protein in the ribosomes. The water plus metabolism causes the radical part of the embryo to elongate and the germination process has begun.
Two potential problems can stop this process. The seed may no longer have sufficient structural integrity, possibly because the aging process while dry no longer maintained the metabolism needed for maintenance. A second problem can be that the imbibitional process caused breaks in the membranes that were not adequately repaired during those first few hours of swelling as water moved into the cells. Membranes do have the capacity to self-repair and often do when metabolism is active. However, this process is temperature related, and in corn this repair process is very slow when temperatures are at about 50°F. Imbibitional chilling injury is the term used to reflect poor germination of some seed when planted in cold soils.
Every seed within a lot, although genetically identical, has had a slightly different environment experience. Location on the ear, exposure to insect or fungus, location in the drier, handling in the sheller or bagging processor all could affect its tendency to cellular injury. This usually if most profoundly expressed when it imbibes water under cold conditions. Some seed may reflect this by only delaying the germination as it repairs sufficient membrane for metabolism to germinate although later than the other seeds.
From Corn Journal 03/08/2018
It is sad that we, and corn seed, age. The mechanisms between us and them may be similar in that mitochondria are probably involved in all deteriorating living cells. These organelles which can number a few hundred in a cell, are the main sites for transformation of stored carbohydrates into useable energy for other cell functions. Mitochondria have their own DNA and are composed largely of membranes. Dehydrated seed results in mitochondria functioning at a very low level resulting in being unable to repair deteriorating membrane structures. While at very low kernel moisture levels (6-14%?) and cool temperatures (less than 50°F (?) further damage is limited. Precise moisture percentage and temperature for best storage of maize seed probably varies for genotype and seed condition but the general concept remains.
Seed imbibition of water is a physical phenomenon with little inhibition from the pericarp or seed coat. Seed treatments added to seed can slow down the imbibition, apparently giving the renewed mitochondrial function more time to repair damaged membranes. On the other hand, only increasing kernel moisture slightly can cause more membrane damage to occur, but not repaired. Increasing moisture more while at low temperatures (50°F) has the same effect. Corn seed planted in cold soils will imbibe water but the low temperature inhibits normal cell function, including repairing mitochondria. Those individual seeds with the most mitochondrial damage are likely the ones that struggle to germinate when the soil temperatures do heat up.
Seed producers are aware of the significance of inadvertently adding a small amount of moisture, such as from a seed treater before bagging by designing their process to limit the water and allowing for drying after application. I recall a case in the Thailand in which a new fungicide seed treatment was applied to control downy mildews but the humid environment did not allow the seed to dry after application. Seed germination quality quickly deteriorated as a result. Accelerated aging test of corn seed is based upon placing seed in an environment of 100% humidity and 113°F for 3 days, then planting in germination test to record the reduced germination. It is intended to predict the viability of the seed after storage. It is notable that even under this condition, all seed within the sample are not equally affected. Some germinated normally, some eventually and some not at all. This is typical of normal, well treated aging seed lots. Each individual seed is in a slightly different condition. We expect maximum performance when emergence is uniform. Seed quality is a factor influencing this trait.
From Corn Journal 3/16/2017
We all want things to be simple but it is amazing how rarely this happens
After overcoming the leaf surface protection against fungal invasion, the battle inside the leaf begins. This corn journal blog in 2018 illustrates the next phase of the battle between host and pathogen.
A recent report in Science (Vol.359, 1399-1403) describes how a single fungal gene controls plant cell-to-cell invasion by the rice blast fungus. It is an interesting description of how a plant pathogen manages to invade a plant cell and manages to travel cell-to-cell, evading the plant immunity system, eventually killing significant sufficient tissue to sporulate and spread to other plant tissue. This study involved a lot of biochemistry and microscopy and uncovered interactions that are probably common to other fungal-corn interactions.
Living plant cell walls have microscopic holes, called plasmodesmata, that allow passage of sugars and proteins to adjacent cells. These holes are smaller than normal fungal filaments (hyphae). In this study in which the pathogen Magnaporthe orzae, cause of rice blast disease, initially invades the plant by forcing the outer leaf cells with an appresorium, to occupy a cell but maintaining the cytoplasm in the cell. The hyphae of this fungus reduce the size of the hyphae to about 1/10th to squeeze through the plasmadesmata into the next cell. The plant cell resistance includes reacting to the presence of the invader by depositing callose to close the plasmodesmata, and therefore restricting the fungus to the initially invaded cell. The researchers found that a single fungal gene delays the resistance reaction until the pathogen has passed on the next cell. Mutants of this gene in the fungus are not able to pass onto the next cell. Resistance is related to a quicker reaction in closing the plasmodesmata as well as repression of the fungus within the infected cells.
This study involving the interaction between a fungal pathogen and host is probably common to many leaf diseases. Relatives of this fungal species attack other grass crops such as wheat and barley but apparently not corn. The study illustrates the evolution of methods of attack by pathogens and competing defense systems by plants. It is also interesting that the study was done by several specialists employing multiple techniques and understandings of their science.
The continual battle between the carbon producer, like corn, and the organism seeking carbon nutrition involves biology of both organisms. Each corn pathogen has evolved different biological features for success. Exserohilum turcicum, the fungus causing northern leaf blight of corn produces spores (conidia) with thick wall that do not immediately desiccate, germinate within a few hours of exposure to moisture and set up an appresorium and penetrate the leaf surface within a single day. The relatively heavy spores tend to not travel far within a field from the original infection site.
Cercospora zeae-maydis, cause of gray leaf spot, by contrast has relatively thin-walled conidia that germinates on leaves with only high humidity (80-90% RH). After germination the mycelium remains on the leaf surface until being exposed to 95% humidity for a total of nearly 100 hours. The mycelium can tolerate as low as 60% humidity in a somewhat dormant and then continue to grow when higher humidity returns. After meeting the minimum, an appresorium forms and the fungus enters to leaf surface. The thinner walled spores of Cercospora zeae-maydis is more easily moved in the winds and therefore spreads easier within a field.
Common rust fungus, Puccinia sorghi, is even more easily spread in the wind. Spores (urediniospores) have thick walls but are round and about a third the size of the E. turcicum spores. Thick walls prevent desiccation allowing long distance travel and light weight encourages it. The spores cannot withstand the absence of susceptible hosts between live corn presence during the temperate winters. Consequently, production of a new urediniospores occurs in more tropical areas with continuous corn growth. High altitude winds carry the spores to the temperate zones where new corn plants are growing. These spores quickly germinate in moist corn leaf surface, germinate, then an appresorium above a stomata, penetrating the leaf. This requires about 6 hours of moisture. The leaf whorl, always moist, fits this process. New spores are quickly produced and spread within the field can happen quickly.
These are three examples of corn fungal leaf pathogens with different infection and biology.
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 be part of quantitative resistance or 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.
Much is written about this disease. An interesting summary of the morphology aspects is included in this report: Journal of Applied Biosciences (2008), Vol. 10(2): 532 - 537. ISSN 1997 – 5902: www.biosciences.elewa.org (From CornJournal 11/21/2017).
Corn leaves are constantly surrounded by fungal spores during the whole season. The waxy leaf cuticle and tight compaction of the epidermal cell walls inhibit penetration by the vast majority of fungi. Even entrance into the leaf through open stomates is restricted by antimicrobial fumes from the cells inside the stomata.
A relative few fungi have methods to overcome these defense systems. Spores of Exserohilum turcicum, the pathogen causing northern leaf blight, germinated within a few hours of exposure to moisture on the leaf. The hyphae growing from the spore responds to the surface hardness producing mucilage promoting adhesion to the leaf surface. Soon the tip of the hypha forms a special cell called an appresorium. Exposed cell wall of the appresorium cell thickens but the wall adjacent to the leaf surface remains thin. The cell gains turgor pressure from moisture as cytoplasm in appresorium cell absorbs glycerol from the fungal spore hyphae. Turgor pressure results in formation of new cell that forces through the leaf cuticle and through the epidermal cell walls.
Penetration into the corn leaf by the pathogen causing northern corn leaf blight occurs about 10-12 hours after the spore and moisture on the leaf surface. Favorable environment for spore germination and appresorium development usually is present in the whorl of pre-flowering plants, with fog, high humidity and dew formation.
The battle between plant defense systems and pathogen offense continues.
Resistance to leaf diseases in corn that limits the number and size of lesions is called horizontal or quantitative resistance and usually involves 3-5 genes. Ratings for this type of resistance involve a scale developed after considering disease pressure from different environments but does provide a stable type of resistance. Resistance to some leaf pathogens can have another system, usually involving a single gene, that stops some races of a pathogen more completely than horizontal resistance. This latter type of resistance is called vertical or qualitative resistance.
The Ht1 gene was discovered in 1964. It prevented the northern leaf blight pathogen, Exserohilum turcicum, from developing the normal wilted lesion symptom after it reached the vascular tissue. Instead of the normal lesion formation, a small yellow streak developed and, most importantly, the fungus failed to reproduce with spores capable of spreading the disease within the corn field. This seemed ideal in the USA because its presence was easily identified and damage from the disease was eliminated. Consequently, the Ht1 gene was utilized in commercial hybrids during the 1970’s. In 1979, a race of this fungus was found in several locations in the U.S. Corn Belt that overcame the Ht1 gene resistance, resulting in normal lesion and sporulation. It appears that the fungal gene responsible to overcome the Ht1 gene was present in a low frequency within the widespread population of E. turcicum. Its frequency increased as it gained competitive advantage over those individuals without this gene. Similar races of this fungus had already been noted in South Africa and the Philippines.
Other single genes (Ht2, Ht3, Htn) for resistance to E. turcicum have also been identified, as well as races of the fungus that overcome those resistance systems. This is not a new phenomenon. Genetic diversity within pathogens have repeatedly shown an increase of individual genes producing products to overcome single gene resistance. It should be noted that the term race for a pathogen refers to only a single gene difference within the pathogen population. It probably existed as a mutation, allowing a slight structural change in a protein that happened to be attacked by the host plant’s resistance product. Qualitative, vertical resistance to a disease in corn offers quick answers but stable, long-term benefits are best when quantitative, horizontal involving several genes are employed in corn hybrids.
Leaf epidermal cells 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.
Characterization of horizontal resistance level to a pathogen requires a rating scale that has some consideration of disease pressure and relativity to other varieties. It is best done when each variety is exposed to the same pathogen intensity at the same stage of leaf maturity. Differences expressed as lesion numbers, size of lesions and percent of leaf destruction can be used to indicate the level of general resistance to that pathogen. I prefer to make ratings based upon several plants exposed to the pathogen in what I project to be somewhat heavy disease pressure in most USA corn environments. With artificial exposure to the pathogen by placing spores in the plant whorl, each plant receives more-or-less the same pressure. Expression of resistance will show 1-2 weeks later. Those varieties with abundance of larger lesions are deemed more susceptible than those with fewer and often smaller lesions. Consequently, it is assumed that will simulate the reactions in fields with somewhat heavy pressure from that pathogen.
Any evaluation of horizontal resistance includes consideration of disease pressure and relativity to other varieties. (Corn Journal 7/11/2017)
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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.