Sugars transport to maize endosperm
Sugar manufactured via photosynthesis in leaves begin as 6-carbon structures (hexoses), primarily as glucose and fructose. These two may be combined to form sucrose. These are the primary sugars transported through the phloem to the developing kernels. Transportation is driven by energy and osmotic pressure and influenced by the cytokinins produced by the new kernel embryos.
Studies concerning the entrance of these sugars into the embryos is usually done with only a few genotypes and probably represent only general principles. Sucrose tends to accumulate more in the embryo but glucose and fructose molecules tend to be more dominant in absorption in the corn endosperm. There are indications that the sucrose is broken into its two components, glucose and fructose, before entering the endosperm cells.
It is difficult to imagine all the genetics that got this human-derived species to this point. Genes affected root efficiency in absorbing minerals and water, leaf size and structure, photosynthetic efficiency, flowering timing, disease resistance and movement of the energy captured by photosynthesis to allow all of this to happen. And now the human objective of capturing excess sugars in the grain involving more genes for the final deposition. It is estimated that corn may have 40,000 genes. The complexity of reaching this point, and the variability for all the parts of this process that is visible to us plus those invisible physiological steps that gets the plant to this point is supportive of this estimation.
Starch formation in kernel endosperm
Glucose from leaves and stalk tissue reserves rapidly move to the kernels, especially in days 10 to 40 after pollination. Most is deposited in the special organelles within endosperm cells called amyloplasts. These plastid structures have their own genome, and like chloroplasts in leaf cells, are believed to have been derived by blue-green algae. Amyloplasts are found in other plants tissues such as fruits and potato tubers. They specialize in conversion of glucose, and sucrose, molecules into the more complex and less water-soluble starch molecules.
Synthesis of starch in corn endosperm amyloplasts involves a series of chemical reactions driven by at least three critical enzymes. Several hundred glucose molecules are joined together in branched molecules to form amylopectin. Normal corn endosperm amyloplasts also have enzymes to join glucose molecules in non-branched, more compact molecules called amylose. Amylose, perhaps because of it compactness, is less easily digested into its glucose components than amylopectin. The branching and non-branching aspects of these two starch molecules in corn endosperm affect eventual human uses of corn as food, animal feed and industry. For example, amylose is less soluble in water, making it more useful as a gelling agent in foods.
Most corn endosperm starch is composed of about 70% amylopectin and 30 % amylose. Genetic mutants can dramatic change to ratio into more amylopectin (waxy corn) or more amylose ( high amylose corn).
Sugar storage in corn stalks
Inner parts of a corn stalk are composed of vascular bundles and large living cells called parenchyma cells. Movement of sugars produced by photosynthesis in leaf cells move to the phloem cells. Concentration of sugars causes water to move via osmosis into those phloem cells, putting pressure for movement of the soluble sugars through the small connections (plasmadesmata) between phloem cells. Digestion and respiration in the growing points of the roots and eventually the newly pollinated ear ovules, with the assistance of cytokinins, directs the pressure towards the root through the stalk.
Large pith cells adjacent to the phloem cells become storage locations for sugars as the plasmadesmata connect between the parenchyma cells. These glucose and sucrose sugars accumulate in the stalk pith tissue. This storage reaches its peak shortly after pollination when the direction of flow switches to the newly formed kernel embryos. Sugars in stalk pith cells become a reserve that allows a constant movement to developing kernels, despite short-term reduction in photosynthesis because of cloudy weather or even the more long-term damage from leaf disease or insects. Although some of the sugars are utilized in cellular metabolism of the pith cells, the excessive accumulation becomes essential to maintaining life in root tissues as well as warding off potential stalk pathogen invaders.
The 50 days of grain fill causes a drain on the sugars stored in the stalk parenchyma cells. Genetics and environment affect the corn plants ability to produce sufficient photosynthates to meet the demand for sugars to flow to the ear. The genetic complexity of this is huge. It must involve factors affecting photosynthetic rates, efficiency of movement of sugars, storage capacity of pith cells, size and structure of roots and size and number of kernel embryos.
Given the variable environments and multiple genetics for corn grain production we should not be surprised that no single corn hybrid is perfect every year in every field
Translocation of sugar in stressed corn
Movement of materials within a plant is called translocation. Minerals are translocated from the roots to leaves through the xylem portion of the plant vascular system. Soluble sugars produced in chloroplasts in leaf cells moves through cytoplasmic connections into the living phloem cells of vascular tissue. The flow direction is guided by hormones such as cytokinins. After pollination, much of the translocation of sugar is directed to the kernels. Tracing the direction and timing of flow is often done by using radioactivity such as radioactive N in nitrate uptake in roots (Plant physiology 100(3):1251-8 · December 1992).
A study published nearly 40 years ago (Plant Physiol. (1978) 52, 436-439) compared the movement of sugar movement from leaves to developing kernels when the plants were under drought stress. The section of leaf tissue was fed radioactive 1CO2 in plants either stressed by root pruning or restriction of water to the plant. Radioactive carbon was incorporated in sugar by photosynthesis at about the same rate in stressed and non-stressed plants. This indicated that rate of photosynthesis was not being affected by the drought stress.
Sugars were translocated to the kernels, stalk near the ear node and the ear shank and husk. Two hours after treatment with the radioactive carbon dioxide, 7.6% of the radioactive carbon remained in the treated leaf area of the non- stressed plants but 20.5% remained in the water stressed leaf tissue. 18.6% of the carbon was moved to the kernels in the non-stressed plants but only 11.0% in the stressed plants. Similar differences were found for the stalk and ear shank distribution.
This study indicated that the effect of drought stress after pollination was greater on the movement of the sugars from leaf tissue than reduction in photosynthesis. Maintenance of living tissue in stalks by translocation to that tissue during drought stress is probably significant as well.
Leaf senescence and leaf disease
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 Fusarium species, 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.
One of the obstacles to evaluating and presenting precise resistance ratings for a disease is relative leaf senescence among corn hybrids. Add this to environmental factors and pathogen intensity pressures and races and one should only expect that disease resistance ratings are not precise predictors of damage from a leaf disease.
Water and corn biology
Water has a complicated interaction with corn physiology and function. It moves through root hairs via osmosis, water moving from a high concentration through cell walls where sugars and minerals reduce the water concentration. It is a physical phenomenon. Osmosis further causes water molecules to move to the xylem vessels. This pressure pushes water up the vessels. Leaf stomata open during the day because photosynthesis in the two curved cells surrounding the produce sugars resulting is swelling, again due to osmosis drawing in water. This causes opening to the air, allows movement of CO2 into the leaf and oxygen into the air. Water evaporates in the opening below the stomata, moving into the air, again moving by relative concentration of water molecules. Dry and windy air increases the rate of transpiration. Water molecules tendency for cohesion, causes water to be pulled upwards, as each molecule transpires through the stomata is replaced by a molecule pulled from the xylem. It's a push from below the soil surface and a pull through the stomata that moves water through the plant.
During cell elongation, before flowering in corn, water movement into new cells largely determines length of cells and ultimately affects plant height. At flowering, this cell elongation process become critical to the timing of ear silks pushing out of ear husk tissue for exposure to pollen. Pollen production and distribution is less dependent on water concentration and therefore timing of pollen and exposure of silk may not match. Poorly pollinated ears are the result of drought conditions.
Photosynthesis utilizes water as H2O is combined with CO2 to make glucose (C6H12O6). Drought conditions during the growth period can reduce ultimate leaf area and thus photosynthesis. Severe drought can result in stomata not opening, reducing the CO2 available but this appears to be most significant before pollination. The biggest cause of grain yield loss from drought stress is not reduction of photosynthesis but it is the lack of place to put its products.
Movement of the glucose from the leaf tissue to grain is determined mostly by the hormones produced in the newly formed embryos in the pollinated ovules. Lack of water reduces elongation of silk causing them not to be exposed to pollen and consequently fewer embryos. Sugar molecules accumulate in leaf tissue, triggering production of anthocyanins in leaves, turning the leaves red. The pigment change reduces photosynthesis.
Corn biology is dependent upon adequate water supply for nearly all functions from being a solvent for movement of sugars and minerals, providing turgor pressure for cell expansion, a coolant as it evaporates from leaf tissue and contributor to photosynthesis.
Virus infection in corn
Viruses are simple particles consisting of a nucleic acid surrounded by a protein. They are totally dependent upon on host metabolism for replication. They have no means of overcoming the physical barrier of the leaf cuticle without assistance of either an insect vector or being physically rubbed into the leaf. Aphids, leafhoppers, plant hoppers, mites and beetles that feed on corn are frequent vectors of corn viruses, each being very specific for the vector species.
After being inserted into the corn cell by the vector, the virus uses its nucleic acid component, a single stranded RNA in many corn viruses, to utilized the host cell’s metabolism to replicate the virus nucleic acid and protein coat. Often this is done near the cellular membrane which is connected by a strand through the cell wall called a plasmadesmata to the adjacent cell. This allows the virus to move cell to cell within the corn plant. These channels function to move materials between cells in plants, including the very small virus particles.
Pathogenic viruses often cause local chlorosis, resulting in yellow streaks and mosaic patterns on the leaves. If the virus reaches the meristem it results in significant stunting of the plant as it interferes with normal cell duplication and cell elongation. This severe reaction usually requires initial infection to occur before the V6 stage of corn development. This timing is dependent upon the timing of invasion by the vector and its infection. For example, late planted sweet corn is more likely to be infected with Maize Dwarf Mosaic Virus because the aphid vector population increased on earlier planted corn now can feed on young corn plants.
Resistance to corn viruses is very specific to each but again the genetic variability in maize results its presence. The more difficult virus diseases such as corn lethal necrosis involves two viruses, maize chlorotic mottle virus, transmitted by rootworm beetles, including their larvae, and additional virus such as maize dwarf mosaic virus, transmitted by corn leaf aphid or wheat streak mosaic virus transmitted by wheat curl mite. Biology of corn virus diseases is often further complicated by alternate plant hosts to the virus. Johnson grass is a perennial host to both maize dwarf mosaic virus (transmitted by aphids) and maize dwarf mosaic virus (transmitted by a leafhopper) the combination of which causing severe damage to nearby susceptible genotypes.
With a little time, corn breeders identify the genotypes with reasonable resistance to each of the new virus diseases, as illustrated with the recent corn lethal necrosis outbreak in East Africa. We can be grateful that corn has broad genetic diversity.
Bacterial infection of corn leaves
Of the multitudes of bacteria species that feed on dead plant tissue only a few can enter the corn leaves. Most bacterial require a moist environment to duplicate and to avoid desiccation. Leave epidermis and its waxy cuticle covering inhibits most bacterial from entering the leaf.
Stomata, while open during daylight, are vulnerable to invasion by bacteria but relatively few bacteria species become established through them. Stomata are a low percentage of the surface of a leaf, decreasing the probability of stomata being exposed to potential bacterial invaders. Bacterial species capable of entering stomata tend to be those with swimming structures such as in the Xanthomonas and Pseudomonas genera, although only a few species of these genera appear to enter the corn leaf. There is evidence in other plant species of some stomata temporarily closing when exposed to bacteria. In these cases, the stomata would be closed for a few hours, only to open later. There is also evidence that some variants of the bacteria produce chemicals to inhibit their detection, effectively negating this defense system.
Bacterial stripe, caused by Pseudomonas andropogonis and chocolate spot caused by a variant of Pseudomonas syringae are examples of diseases caused by bacteria entering through stomata. Another example is bacterial leaf streak caused by Pseudomonas campestris pv zeae, a more recent disease in the USA but known in South Africa since 1949.
Two corn diseases caused mainly by bacteria entering injured tissue are Stewarts disease and Goss’s bacterial wilt and blight. Pantoea stewartii enters through injury and commonly is vectored by the corn flea beetle as if feeds on corn leaves, inserting the bacteria into the leaf mesocotyl. Goss bacteria (Clavibacter michiganensis subsp. nebraskensis) mostly are associated with hail leaf injury in which infected debris from a previous crop are exposed to inner leaf tissue.
After entrance in the leaf tissue, the bacteria utilize intercellular nutrients and moisture to multiply, killing cells as well. Eventually the host plant’s resistance system limits the destruction. Resistance genetics varies among inbreds and hybrids, with relatively few incapable of stopping these bacterial from causing significant damage.
It is a dynamic battle between potential pathogens and corn plants.
Quantitative disease resistance
Resistance to corn diseases is the result of the plant tissue recognizing the invasion of the pathogen and responding by turning on the resistance mechanism. There are multiple corn plant genes involved and thus the term quantitative gene response is used to reflect the genetics. A recent research paper (Nat Genet. 2017 Jul 24. doi: 10.1038/ng.3919.) identified a single gene coding for an enzyme critical to lignin production. Lignin is a component of cell walls, suggesting that presence of this gene causes the cells, at least in the region of the infection to produce a physical barrier to the pathogen. This gene was found associated with resistance to the pathogens causing southern corn leaf blight, northern leaf blight and gray leaf spot. It is assumed that this gene is not the only gene involved but does contribute to limiting the lesion size that develops from these diseases.
Most corn leaf fungal pathogens, other than those causing rust and smut diseases, receive primary nutrition from dead plant tissue. Their ‘strategy’ is to kill tissue, get nutrition, produce spores and then spread to new leaf tissue to repeat the cycle. Quantitative resistance in host plant strategy is to limit the area and slow the advance of the lesion. Corn varieties may differ in number and size of lesions when under identical disease pressure but even those with relatively good ratings for quantitative resistance can be damaged if pathogen pressure is high because of carryover diseased tissue and environment favors the pathogen. This is the reason that most disease resistance ratings need to consider pathogen pressure.
Although there may be some commonality among resistance to various pathogens, other genes participating in quantitative gene resistance can be more specific to a pathogen. Perhaps it involves gene products associated with recognition of a specific pathogen. Although the gene sited above may be part of the resistance to three different pathogens, other genes may affect the response to each one of these. Good resistance to the gray leaf spot pathogen does not assure good resistance to the northern leaf blight pathogen.
Physiological status of the corn plant also affects it ability to react to a pathogen. Leaf diseases often show greatest a few weeks after pollination, probably because leaf tissue is moving carbohydrates to the ear and cells begin to senesce. Lower leaves of the plant, being the oldest and receiving less light are at a lower physiological state than upper leaves.
Varying disease pressure and plant maturities complicates establishing disease resistance ratings of hybrids. The main attempt must be to distinguish those with extreme susceptibility from those with intermediate and very resistant levels to the level of each disease the hybrid could be exposed.
Helminthosporium carbonum races
Among the fungi that are usually barely pathogenic on corn is a relative of the one causing southern corn leaf blight. The old name for this fungus is Helminthosporium carbonum and the most recent name is Bipolaris zeicola. It has slight spore structure and pigment differences from the cause of southern corn leaf blight (Helminthosporium maydis = Bipolaris maydis) and traditionally was found more common in the northern parts of the US corn belt. This fungus is a common inhabitant of many grasses and host resistance usually restricts the fungus to feeding on dead or senescing leaf tissue. H. carbonum and H. maydis have similar sexual reproduction structures, causing fungal taxonomists to place them in the genus Cochliobolus. H. carbonum, thus is Cochliobolus carbonum and H. maydis is known as Cochliobolus heterostrophus. Sex within a species provides new genetic combinations, including single gene combinations that can fit with single gene changes in hosts, resulting in a traditionally weak pathogen such as Helminthosporium carbonum to become an aggressive pathogen.
In the late 1930’s, a race of H. carbonum was found that produced a toxin on specific corn varieties, resulting in large leaf lesions and significant moldy corn grain. Now we had race 0 for the traditional form of the species and race 1, defined as producing the HC toxin.
I came into the seed industry as a mycologist in 1972, immediately after the H. maydis Race T epidemic. I and many other corn pathologists in the summer of 1972 found a wide range of lesion types on corn inbreds in breeding nurseries with fungi producing spores that looked intermediate between H. maydis and H. carbonum but not restricted to the T sterile cytoplasm genetics. Apparently, the large distribution of H. maydis in 1969 and 1970 allowed the sexual crossing of the two species, resulting in multiple new combinations of the two related fungi. Within the next 20 years these segregating fungal populations became sorted into more distinct races of H. carbonum. The races are defined by the symptom and are generally host specific. Race 2 tends to result in oval-shaped leaf lesions on inbreds and hybrids with susceptible genetics, often with inbred W64 background. Race 3 is defined by giving very narrow lesions, again on specific susceptible host genetics (B73). Race 4 was defined in 1990 by the oval shaped leaf lesions on B73 backgrounds but not on W64 genetics.
It is notable that these ‘races’ were probably only differences in a few fungal genes and that the hosts were specific inbreds. Corn hybrids usually were not significantly affected because of dominant resistance in one of the parents but they did cause problems for seed producers. Race 1 is the most destructive of these H. carbonum races because of its toxin. It also still exists, and occasionally shows up in breeding nurseries when a susceptible genotype occurs. It is an advantage to have it show up in a nursery. Seed fields scattered across multiple central USA states were suddenly affected by Race 1 in the 2014 growing season. All had the same or closely related inbreds. A summary of Cochliobolus carbonum can be found at https://en.wikipedia.org/wiki/Cochliobolus_carbonum
Genetics of corn and of potential pathogens interactions are constant.
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.