Corn, like most grain crops, is grown mostly for carbohydrates as a source of energy. Most of the carbs are stored as starch in the endosperm component of the kernel. Protein, which makes up only about 8-9 percent of the kernel, is mostly located in the embryo. Grain starch is composed of two types, both being composed of glucose molecules. Glucose is a relatively simple molecule composed of 6 carbon, 12 hydrogen and 6 oxygen atoms. Amylose type starch is mostly a linear string of several hundred glucose units. Amylopectin, the other type of starch component, is a more branched but shorter type of starch. The two types of branching result in differences in ease of digestion, amylopectin being easier to digest apparently because of the shorter structure. Amylose appears to be a little more efficient for storage in plants because of its linear structure. The differences in the two types of structure affects their properties as well. Amylose tends to be less soluble in water and can act as a binding agent in gels. Amylose does bind with iodine, causing a blue color when exposed to iodine. Most dent corn hybrid starch is about 25% amylose and 75% amylopectin.
A single recessive gene can cause corn to produce mostly amylose starch, with some modifier genes affecting the actual percentage. Because it involves a recessive gene, both parents of the hybrid must be homozygous for the recessive gene and the hybrid field must be isolated from normal corn to maintain the purity. Waxy corn starch is totally amylopectin and also controlled by a single recessive gene. Consequently, both parents of the hybrid must be homozygous for this recessive gene and isolation of the hybrid field is needed to keep the grain quality. Amylopectin does not stain blue with iodine. Both types of starches have separate commercial uses.
Atmospheric carbon dioxide concentration drops drastically during the corn growing season in the USA Midwest. Corn, being a C4 photosynthesis plant, is an especially big consumer of carbon dioxide and today’s culture of planting high density crops, increases the consumption. One estimate is that a field with 210 bu/A yield sequesters, per acre, about 3.6 tons of carbon is in stalks and leaves, 3.6 tons in roots and another 3.6 tons in kernels. Obviously these actually vary per hybrid and environment but a corn field does tie up more carbon dioxide during the growing season than a tropical forest. However, the roots and above ground foliage does return the CO2 as microorganisms digest the components. If grain is processed through livestock, or humans, or ethanol it eventually also gets released. Although the forest trees delay the release for many years, eventually that carbon is also released as the wood rots or is burned. Even in the forests where carbon is being deposited as wood, those deposits during the past are rotting by micro-organisms, releasing carbon dioxide.
Plants grown today consume carbon dioxide in today’s atmosphere and return it in a relatively short time. Fossil fuel carbon was tied up a few hundred million years ago during a time of a warm and very wet earth. Some of that carbon did not cycle but, over time, the dead plant material was covered with deposits of sand and soil. Use of fossil fuels are new contributions of CO2, beyond the recycled CO2 that is done by current plants. Recycling of current CO2 should not be confused with addition of CO2 from fossil fuels. Methane release from livestock is only part of the CO2 currently present and not contributing to the increase. Ethanol produced from corn stalks or grain substituted for fossil fuel can reduce the addition of CO2 to our atmosphere.
Corn borer infestation has been associated with stalk rot but probably not in the same way that some have inferred. Second brood larva of the European corn borer makes a hole through rind and then a tunnel in the pith. Some have conjectured that this allows fungi to enter the stalk but actually the fungi associated with stalk rot are restricted by living pith cells, regardless of how the fungus gets into the tissue.
The borer can weaken the stalk causing it to break. If it lodges below the ear, then the remaining stalk will not be rotten. However, if the breakage is above the ear before completion of grain fill, the lower stalk will be brown and rotting. The borer did not cause stalk rot by allowing the fungus to enter the stalk but instead is associated with stalk rot by preventing, after lodging, photosynthesis in the upper leaves. Consequently, insufficient carbohydrates are available to fill the kernels and keep the roots alive. The plant wilts as the root tissue dies and stalk rot fungi invade the wilted stalk tissue. This affect can be produced artificially by cutting the leaves off the corn. The more leaves cut above the ear after pollination. the higher the percentage of plants with stalk rot. If the stalk is cut below the ear node, there is no yield but also no stalk rot.
The same phenomenon is involved with corn borer damage and occurrence of stalk rot.
2,4-dihydroxy-7-methoxy-1,4-benzoxazin-3-one, also known as DIMBOA is known as insect growth inhibitor in corn. It has been shown to reduce the digestibility of food by European corn borer by acting as a digestion toxin. DIMBOA degrades into a related product in corn called MBOA that reduces the digestibility of food in the corn borer. Not all varieties produce the same amount of DIMBOA. In the popular hybrid B73 x Mo17, B73 was very low in DIMBOA content and Mo17 was very high. The hybrid was intermediate to these two parents. Selection for higher DIMBOA content was shown to be possible. Highest concentration was in young plants, including the roots.
Fall armyworm (Spodoptera) have been shown to detoxify DIMBOA but the plant responds by synthesizing a related compound (HDMBOA-glc) to defend against this insect (Plant J 68: 901–911). Another indication of plant’s metabolic interaction with potential predators.
High concentrations of DIMBOA in the corn root tissue are released into the soil surrounding the root tissue. This inhibits some potential pathogens of the root. A few beneficial bacteria have evolved tolerance to DIMBOA, allowing them to invade and dominate the area around the corn roots. (http://dx.doi.org/10.1371/journal.pone.0035498)
There is a lot of unseen biology going on in a corn field.
Damage from European Corn Borers in the U.S. Corn Belt has been minimized by use of the Bt genes. Although the damage from this pest has been most noticeable with stalk breakage and ear drop, early feeding also has been shown to cause yield loss. First brood leaf feeding can interfere with movement of water and photosynthates, ultimately leading to poor ear development. Non Bt corn and other grasses do produce defense compounds in reaction to chewing insects, such as corn borer larvae and sucking insects such as aphids.
One group of these chemicals are benzoxazinoids (acronym Bx). These are stored in the cell vacuoles within the cytoplasm. These are at highest concentration in young plants in the roots and younger leaves. After the detection of cell injury by the insect, enzymes are activated to change a precursor called MBOA to the active form called DIMBOA. This chemical negatively affects the insect’s ability to digest the leaf contents and thus reduces the damage of the first brood. Varieties vary in DIMBOA content and all plants have a reduced concentration as they approach flowering.
Production of DIMBOA in plants does carry an energy cost and genetics involved is complex. Genetics for DIMBOA production involves several genes with hybrids expression being intermediate between the parent inbreds.
There are varieties with less DIMBOA that still express first brood resistance. This appears to be related to cell wall components such as lignins and pectins, apparently making the tissue less easily digested.
There is energy expense associated with all forms of insect and microbe resistance. Some of this cost is reduced if the final product is produced as a response to the invader as opposed to being always present but I am not aware of a comparison of the energy cost of Bt versus more complex induced systems. Certainly the Bt system involving only a single gene is easier from the corn breeding point of view.
Distinguishing between these two types of lodging is important to making future crop decisions. Late season stalk rot features breakage of the stalk, usually in the lower internodes. Such plants have brown rind color and hollowed pith areas. Root lodging, on the other hand features intact stalk tissue with green rind colors. Root lodging can occur nearly any time during the season but when occurring near or before flowering the plants tend to recover somewhat with the stalk bending upwards. Root lodging requires strong winds and generally occurs when secondary root did not develop enough horizontal roots to avoid the lodging. Hybrids do vary in this tendency, having differences in root growth direction tendencies. Those with more vertical roots could be better for drought, being able to absorb water at greater soil depths, but have trouble in a highly organic soils especially those that hold the moisture towards the surface. Pest factors such as rootworms and nematodes also influence root lodging.
Stalk lodging due to stalk rot is affected by a different set of factors, as discussed in recent blogs. Leaf damage from disease or hail, cloudy weather, early season rain affecting kernel numbers are predisposing factors to stalk rot. Certainly, hybrids vary in reaction to these factors as well.
Excess moisture before flowering can be associated with both types of lodging in that root development could be underdeveloped and kernel numbers could be increased. Likewise, high plant density can cause reduced root development and less than optimum photosynthesis. Late season storms, with soaked soils favor more root lodging in hybrids with less developed brace roots whereas the moisture reduces the stresses associated with stalk rot.
Distinguishing between the two types of lodging can allow analysis of probable causes and planning for corrections for the next season.
Race T of southern corn leaf blight struck the U.S. corn belt in 1969 and 1970. It was quickly solved by the seed industry making a relatively easy change in cytoplasmic genetics. But a good thing about that epidemic was it caused the seed companies to enhance their disease resistance efforts by hiring corn pathologists. I was a beneficiary of that effort, starting with Cargill Seed Department in 1972. The major leaf blight problem being solved, I asked corn breeders for the most problematic corn disease. Stalk rot was the common answer. It occurred inconsistently across many hybrids and screening methods seemed inadequate. It was a frustrating disease from the corn breeder’s perspective.
I was definitely in a learning mode, educated as a botanist and mycologist but not an agronomist. I did a lot of literature review and visiting with more experienced university researchers concerning corn stalk rot. A group of public and private corn pathologists met annually for 1-2 days to discuss recent research and observations. There were about 25 people in the group at that time, lending the opportunity for presentations that were not really ready for journal publication but feedback from corn disease professionals. I presented my summary of stalk rot ideas to that group in February 1975, including bibliography of published stalk rot research. I don’t recall the precise feedback but I felt encouraged to proceed with experiments to test the photosynthetic stress-translocation balance concept of stalk rot.
The literature illustrates the difficulty in describing the interaction between the physiology of the corn plant and the fungi involved in stalk rot. It also shows the balance of field and lab research done by the researchers of that era, a characteristic that needs to be continued.
Attached is a pdf copy of the 1975 presentation that I gave to the corn disease group. A similar but larger group of corn pathologists continues to meet annually.
This concept of stalk rot was first published in 1977 (Proc.32nd Annu. Corn and Sorghum Res. Conf. 32:122-130 and followed by publication of evidence of kernel number influence in 1980 (Phytopathology 70:534-535). This was a culmination of many studies done by other researchers in the 1950-1973 in which the physiology of the corn stalk was studied. Among the notable publications are:
Senescence of pith cells in corn
BeMiller, J.N. and A.J. Pappelis. 1965. Phytopathology 55: 1237-1240
Miller, T.L. and O. Myers. 1974. Crop Sci. 14:215-217
Pappelis, A. J. 1965. Phytopathology 55: 623-625
Pappelis, A. J. 1970. Phytopathology 60:355-357
Craig,J and A. L. Hooker.1961. Phytopathology 51:376-382
Photosynthesis rate and stalk rot
Earley, E.B. Et al. 1966.Crop Sci 6(1):1-7
Moss,D.N. and H. T. Stinson, Jr. 1961. Crop Sci. 1:416-418
Photosynthesis and root rot
Crapo, N.L and R.G. Bowmer.1973. 01KOS 24:465-468
Leaf removal and stalk rot
Littlefield, L.J. 1964. Plant Dis. Reptr. 48:169
Gates, L. F. and C. G. Mortimore. 1972. Can. J. Plant Sci. 52:929-35
Science builds on science. These studies and others done 40-60 years ago laid the groundwork for us to understand the dynamics of corn stalk rot as it occurs today.
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.