Ht1 gene for resistance to Exserohilum turcicum, cause of northern corn leaf blight, was incorporated in most US hybrids during the 1970’s. This gene was responsible for reacting to initial infection by this fungus by producing a toxin to the fungus in the area of infection that prevented the fungus from producing spores to spread the disease to other plants within the field. In 1979, it was reported that a seed field of corn with that gene had been attacked by E. turcicum producing lesions with spores. Inspection of fields in many locations in the USA discovered the same phenomenon. A gene in the fungus, apparently not previously frequent among the genome, was greatly favored over those variants of the fungus with limited production due to the Ht1 gene in corn, had built up an intensity until it was noticed by the right humans to identify the new race.
This type of genetic battle between host species and potential pathogens is continual. Most potential pathogens are controlled effectively by resistance mechanisms in corn either intentionally by corn breeders screening for resistance when the crop is intentionally exposed to the pathogen. Most damage occurs when new environments favor a variant of the pathogen that allows it to overcome host resistance systems. It is probable that the pathogen variant occurred for several seasons only to gradually build up intensity to be noticed and identified.
Corn Lethal Necrosis, also known as Maize Lethal Necrosis, develops into a damaging corn disease when Maize Chlorotic Mottle Virus (MCMV) and another virus infect the same plant. Both viruses have separate insect vectors. Although MCMV had not been found in the USA until the outbreak of damage from the disease, it was later found that this virus was found in multiple locations, but absence of other viruses prevented notable disease development.
Race T of Bipolaris maydis, cause of the epidemic of southern corn leaf blight had a gene that attacked the mitochondria associated with male sterility of corn. The bacterium causing Goss wilt probably is a mutant of a common grass pathogen. Pathotype 4 of Bipolaris carbonum, cause of very minor pathogen of corn, had a gene that specialized in attacking a common inbred used in many corn hybrids.
There are multiple examples in the many places that corn is grown where the genetics of the pathogens, the corn and environments result in development of what appear to be new diseases. In all cases, efforts by corn specialists identify these factors and reduce the damage by selection of resistance and/or changing the environment that favors the pathogen.
There is no reason to believe that this will not continue. We benefit from the broad genetics in Zea mays.
The 2019 early corn growing season will probably feature unusual disease movements. Having personally seen many of the diseases shortly after being first identified, I do often reflect on how they got there. Eyespot was first identified in Japan in 1959 but more than 10 years later it was found in North Central USA, Argentina, Brazil, Europe and New Zealand. Was it a minor pathogen (Kabatiella zeae) so weak on corn that it only became noticed after more susceptible inbred like Wf9 and W64A became widely used?
Goss wilt bacterium, Clavibacter michiganensis sp. nebraskensis, was first identified in Nebraska in 1970 where it was especially virulent on some genotypes. Switching to more resistant hybrids quickly reduced the damage but the disease was later found in several states. These pathogenic bacteria were found to overwinter in diseased corn debris but how did it spread?
Corn Lethal Necrosis (also known as Maize lethal Necrosis caused by a combination of Maize Chlorotic Mottle Virus MCMV and either Maize dwarf Mosaic virus or Wheat Streak Mosaic virus was first identified in 1976 in Nebraska and Kansas. The virus had been identified in Peru in 1974. Since then MCMV has been found in Argentina, China, Thailand and central Africa. This virus is transmitted by beetles and thrips. Severe symptoms show only when MCMV plants are also infected with the other viruses. Seed transmission has been shown at an extremely low rate. Resistance has been identified.
Damages races of more common corn pathogens such as race T of Bipolaris maydis, Races 1 and 3 of Bipolaris zeicola, Race 1 of Exserohilum turcicumall were related to use of specific
susceptibility genes. Grey leaf spot became notable as susceptible genotypes became widely used combined with less crop rotation and more previous crop debris.
Bacterial Leaf Streak, caused by Xanthomonas campestris pv. zeae, was first identified in Nebraska in 2016. Previously it was only known to occur in South Africa. Is has since been found in 7 USA State and probably in Argentina. Was it always in these areas as a minor pathogen of other grasses but environment and host susceptibility allowed it to increase sufficiently to be identified? Tar spot has been recently noted in north central states after previous identification in higher altitude South American areas. Caused by synergism of two fungi species, much is still be learned about the disease.
There remains much to be learned on mechanisms of susceptibility, environmental factors and movement of pathogens involved in occurrence of ‘new’ corn diseases. It is a non-ending problem in a widely grown crop.
Midwest corn belt planting delays will affect more than only normal yield dynamics but also corn diseases. Corn escapes damage from viruses such as maize dwarf mosaic because the damage occurs when the virus reaches the growing point before the v6 stage of development. Spread of the virus via aphids usually is limited close to the overwintering source of this virus as the aphids tend to spread further north as the temperatures become warmer. Although the June temperatures in the Midwest in 2019 have been cooler than normal, it seems reasonable to assume the aphids can feed on corn at very early development stages further north than usual. Frequent rains could mitigate this aphid survival affect, however. Other virus vectors likewise may have unusual distributions onto corn young plants.
Fungal leaf diseases, such as northern leaf blight, are usually favored by wet conditions. Sporulation on corn debris from the previous year is encouraged by the frequent rain, water in leaf whorls and high humidity allows quick invasion of leaves in the young plants. A few weeks later these lesions become sources of new spores that are easily distributed by winds to new fields. The dynamics of having later planted fields nearby could produce unusual northern leaf blight pressure, especially on those fields.
Gray leaf spot fungus also produces spores on infected leaves from the previous season, but infection of new crop is more favored by humidity than rain. Will excessive rain in June result in higher humidity than normal for the summer of 2019?
Common Rust and Southern Rust spores are carried in storms originating in the Southwest and Caribbean Islands. Corn is most vulnerable before flowering, as the leaf whorl provides an inoculation chamber for the spores to germinate and infect the leaves. The mix of planting dates within an area increases the potential for damage to the later plantings.
This unusual planting season will provide new disease pressures on corn that will require special attention this summer.
Excessive rain in much of the USA Corn Belt in 2019 with ponds of water in areas of fields can encourage infection by a fungus that has swimming spores. Corn Journal blog of 05/30/17 may be appropriate for this year as well.
One of the effects can be infection by an organism called Scleropthora macrospora. This is a fungus-like organism belonging to a group of organisms called Oomycetes. Also in this group are pathogens causing Downy Mildew and Pythium diseases of corn and other plants. Common among these are the ability to form thick walled spores to withstand stress environments that can release swimming spores when in water-saturated soil. S. macrospora infects more than 140 grass species in addition to corn.
The source of infection of corn is often grasses near a low spot or edge of a field. Oospores in the flooded living and dead leaves release swimming spores (zoospores) when close to the corn submerged leaf tissue these zoospores release a germ tube that infects the plant. The filaments (hyphae) grow towards the meristems throughout the life of the plant. This can initially be seen as fine stripes in the leaves but the most obvious symptom is proliferation of leafy aberrations of the tassel- the crazy top symptom. Scleropthora macrospora also can grow to the ear bud meristem, causing similar multiple ears from a single node- but no grain.
Related oomycetes occurring in warmer, subtropical and tropical environments can cause similar symptoms. These downy mildew diseases can also cause the proliferation of the tassels and ears. Susceptible genotypes can have severe grain loss from these diseases. Scleropthora macrospora infection is usually limited to a very small area near grass in a low part of the field.
Infection occurs when the plants have less than 6 leaves. Symptoms that show late in the season, but the problem began with excessive rain that occurred only a few weeks after planting. That early moisture that may contribute to large yields can allow this pathogen to form these unusual corn structures in a few spots of the field. In addition, it is just part of the interesting biology of corn.
Much of the 2019 corn growth in the USA is erratic due to wild swings in water and temperature, affecting planting timing and plant densities. And that is only what we see! Internally many interactions are also occurring and are affected by these environments.
Much of the above-ground growth for the first 30-40 days after seedling emergence is due to cell elongation within leaves. This not only allows the expansion of leaf blades to increase the mass of leaf tissue, but also elongation of the leaf sheaths, pushing up the plant height. Cell elongation is not only occurring in the outer tissue, but internal cells also grow in size during this time.
Cell elongation is driven by energy allowing production of cell components such as cell wall cellulose and lignin but also increase in the membranes, ribosomes, mitochondria and chloroplasts needed to drive the growth. Immature cells, before tightly constricted by deposits of solid cell walls, expand with water pressure during this growth pressure. Consequently, soil water and root development become major factors affecting the size of the corn plant during this pre-flowering stage. Root development not only affects the absorption and movement of water into these growing leaf cells but also uptake minerals needed for the general metabolism. Expansion of leaf blades during this time also increases the absorption of light driving photosynthesis, providing more energy for cell function and growth.
Multiple environment factors influence water supply to corn plants, but genetics also distinguish variety reactions to growth of the plant. Root size and growth pattern affect water and mineral uptake. Structure of vascular tissue from roots to leaves affect efficiency of water movement. Number and activity of stomata in leaves affect the evaporation of water from leaves. Efficiency and number of chloroplasts within the cells affect the transmission of light energy to carbohydrates, mitochondrial numbers and efficiency affect the change of this energy into ATP for use in the formation of proteins and other products needed for cell growth. Translation of chromosomal DNA to RNA that moves to ribosomes where the codes for specific amino acids are strung together for specific proteins, some of which are used as enzymes driving production of cell structure components. A large number of those 30-40000 corn genes must be participating in that early growth of a corn plant.
It is difficult to predict the final grain production of fields under these circumstances and it is probably that all hybrids will not react the same, even if the principles of biology will apply to all.
After emergence and successful elongation of the first true leaves, photosynthesis becomes the energy source for future growth. Consistent with its tropical origin, corn photosynthesis is negatively affected by low temperatures. Leaves grown at 14°C (57°F) have 30% of the photosynthesis rate as those grown at 25°C (77°F). (Plant Physiol. (1995) 108: 761-767). Much of this reduction is recovered within a few hours if the leaves are returned to the higher mid-70 temperatures.
Light energy absorbed by chlorophyll causes an electron to be moved within the chloroplast but if it does not ultimately get utilized in synthesis of carbohydrates, it can damage a critical protein needed in photosynthesis. Corn chloroplasts react by producing a yellow pigment (zeaxanthin) protein that is active in the quick recovery after the heat returns. Chlorophyll molecules are relatively unstable especially in high light intensity and low temperatures, further contributing to reduced photosynthesis at the lower temperatures.
Another protection system in corn, and other plants, that develops in the cell outside of the chloroplast is the pigment anthocyanin. This red pigment absorbs the blue light spectrum of sunlight and thus reduces photosynthesis. Anthocyanin forms after the sugars reach a high concentration. This often happens in seedlings when sugars are unable to be translocated to the roots, again because lack of the heat energy needed to move the sugars. Hybrids vary in the tendency to produced anthocyanin, occasionally causing alarm to the grower but return to warmer temperatures results in disappearance of the red color and normal photosynthetic rates in the seedling leaves. (Corn Journal, 5/5/2016)
Leaf epidermis cells provide important functions beyond providing a tight layer of cell walls surrounding the inner mesophyll cells of the leaf. Epidermal cells also produce a polysaccharide layer outside the outer cell walls and a fatty acid layer of wax further outside. Synthesis of these cuticle and wax substances begins in plastids within the cytoplasm of the epidermal cells. These newly manufactured compounds are moved via the endoplasmic reticulum eventually being deposited on the outer surface of the epidermal cell walls. The fatty acid wax is moved further outside forming a waxy surface to the cuticle.
Multiple genes are involved in production of these complex molecules as synthesis requires linking simple products of photosynthesis (glucose) with inorganic materials to form new compounds. The basic process is common to all land plants as they adapted to life outside of the aqua environment of algae. Further selection for adaptation to varying corn environments allowed for selection of genetics affecting responses to environmental stress.
Outer wax causes water to run off the surface, taking pathogen spores with it. Chemicals applied by growers usually include a surfactant to overcome the water resistance by breaking the tendency of the water molecules to form drops, thus reducing this feature of wax. Pathogenic leaf fungi enter the leaf either by establishing a ‘drilling station’ on the surface from which hyphae extension (appresorium) is pushed through the wax and cuticle layers on the epidermal cells. Other fungi and some bacteria, unable to penetrate the wax and cuticle, avoid the problem by entering through the stomatal openings.
Wax also prevents water loss. Corn genotypes vary in this response to dry environments, some making thicker layers of wax than others when in a dry environment. Leaf surfaces of hybrids grown in the less humid environments of western corn belt have a different texture than the same hybrid grown in the more humid eastern US corn belt. Wax production differences among varieties is probably one of the components to more drought resistance.
Cell division in the meristem establishes the eventual structure of the new leaves unfolding in the young seedlings. Corn has several unique leaf structures that contribute to it’s ability to be one of the most efficient crops in capturing CO2 from the atmosphere. One contributor is part of the epidermis.
The single layer of cells on both the top and bottom of corn leaves are mostly non-pigmented cells tightly bound together, restricting water loss. Further protection comes from a wax covering the outside of these cells. The exception to this tight wall structure comes from some unique cells interspersed within the epidermis on both sides of the leaf. These cells not only have chloroplasts with chlorophyll but are shaped differently. The two guard cells of the stomata are shaped in a manner that allows only one side of each cell to swell with water, with the affect of making a small pore in the epidermis between the two cells. The swelling occurs during photosynthesis within these cells. This process essentially results in the import of potassium ion into the cells, causing an increase of solutes and thus, through osmosis, transfer of water into the cells. The result is stomata pores are open.
This is essential, of course, to allow diffusion of CO2 into leaves for photosynthesis in other leaf cells. Open stomates allows O2 to be released to the atmosphere but also water loss. Water evaporation through stomates (transpiration) is affected by the relative humidity in surrounding atmosphere as the water concentration within the leaf spaces is nearly 100%. Cohesiveness of water molecules 'pulls’ water up to the leaves so that essentially every molecule of water that goes out the stomata is replaced by one from the root tissue.
During the day, stomata are open, carbon dioxide moves into the leaf, oxygen moves out and so does water. At night, photosynthesis in the guard cells stops, water moves out of the guard cells causing the swelling to be reduced and the pore is closed. More references on the links below.
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.