Among the perplexing interactions in corn is that with corn and the fungus Fusarium verticilloides. This fungus was formerly known as Fusarium moniliforme and is the asexual stage of the fungus Gibberella fujikuroi. Many, (most?) seed samples germinated by paper methods will show at least a few seeds with this fungus growing from them, even with the appearance of normal seed germination. The fungus does produce a toxin called fumonisin that can cause rejection of grain by some livestock and grain elevators. This can occur in kernels showing not symptoms of infection.
The fungus can be found in corn roots, stalks and leaves as well, often without symptoms. It is not unusual to find this species growing from dead corn leaf tissue when moistened. It is as if it is an inhabitant of corn. Does it become transmitted to the next generation from infected seed? It is acknowledged that seed can be infected via growth of the fungus in the silk. Or does it become from infected debris in the soil? Or, perhaps entering thru injuries to plant tissue.
A study published at Appl Environ Microbiol. 2003 Mar; 69(3): 1695–1701 followed the spread of F. verticilloides from infected seed and from inoculated soil through corn plants using a carefully designed group of experiments using fluorescent strain of the fungus detected by fluorescent microscopy. They confirmed that this fungus can infect through the root to the mesophyll, often growing between cells. This can result in stunted seedlings, especially if grown under low light conditions. This growth can advance into the stalk tissue, in leaves and even into the seeds, sometimes without showing symptoms. More of the fungus was found in the plant if the soil inoculum load was increased. There was spread to the roots and to the rest of the plant from infected seed but the soil inoculum load appeared to be more significant.
Low light association with increased symptoms suggests that the metabolic health of the plant affects the defense against this fungal invasion. That also is consistent with the presence of this fungus in nearly all rotted stalks. If other stalk rotting fungi, such as those associated with Diplodia stalk rot, Gibberella stalk rot or Anthracnose stalk rot are not found, we tend to call it Fusarium stalk rot because it is always there. The low physiological state of stressed corn plants as they approach completion of grain fill increase the vulnerability the expansion of this fungus into the dead stalk tissue.
Microbes inhabiting the corn plant reflect the complexity that actually is affecting the biology of the corn plant.
A mature maize kernel is composed of endosperm and embryo surrounded by the pericarp. The embryo has three types of meristems. A root meristem, a shoot meristem and lateral meristems. The initial lateral meristem located at the base of the shoot develops in the early stages of kernel to become the scutellum. The next lateral meristem becomes the first leaf tissue to emerge from the soil. This sheath-like tissue wraps around the other shoot tissue. The next 4-5 leaf meristems are also present in the mature corn embryo, each produced on alternate sides of the shoot. The fact that the coleoptile meristem is located very near and on the same side of the shoot as the scutellum meristem supports the hypothesis that it, like the scutellum is an extension of the same single cotyledon. Kaplan D. R
. (1996). Early plant development: From seed to seedling to established plant. In Principles of Plant Morphology, Chapter 5 (Berkeley, CA: Copy Central, University of California, Berkeley)
The apical meristem of the corn embryo shoot maintains a small group of cells programed to divide and eventually producing new specialized cells. Genes in all embryo cells are inherited from both the male and female parent. Mitochondria and plastid genetics are from the mother plant only. Position on the axis, probably in relation to the attachment to the cob on the mother plant, determines that genes turned on in embryo cells furthest away become shoot meristem and those closest to the base produce root cells. The tissue between the two is regarded as the hypocotyl. This becomes the site of most cell elongation that pushes the shoot enclosed by the coleoptile to exposure to light above the soil. It is also the embryo area of attachment by the scutellum and thus the location for movement of nutrients from the endosperm after digestion in the scutellum into the growing root and shoot cells during germination.
The mature corn kernel includes nutrients in the endosperm, cytoplasmic capability in the scutellum to digest and move these nutrients and embryo axis components of meristems ready to go when environment is available. A more technical summary of the shoot apical meristem can be found at http://www.plantcell.org/content/24/8/3219#ref-list-1
Zea mays belongs to the monocotyledon order of seed bearing plants (Angiosperms). Whereas dicotyledons have two cotyledons enclosed in the seed to provide initial nutrition to the embryo and often emerge to also produce more nutrition via photosynthesis, the single cotyledon of grasses such as corn, remain in the soil with the submerged seed. This cotyledon is called the scutellum. It is a thin, shield-like structure between the rest of the corn embryo and the endosperm. Its primary function is to absorb nutrients from the endosperm and transmit them to the growing embryo. Scutellum genetics are inherited with one set of chromosomes from each of the two parent plants. Mitochondria in the scutellum are inherited from the female parent.
Scutellum tissue is a storage tissue for the embryo, accumulating up to 90% of the kernel oil, 20% of protein and 10% of minerals. These become essential supplies for the germinating root and shoot.
Scutellum tissue is about 90% of the mass of a corn embryo, nearly surrounding the root and shoot growing points of a dormant corn seed. It is attached between these two growing points. A layer of scutellum cells adjacent to the endosperm, during germination, produce and secrete enzymes into endosperm, digesting the starch and proteins. Resulting sugars and amino acids are translocated to the embryo axis from which they are utilized for new cell development in the growing shoot and root tissue. Movement of these substances from the outer edge of the scutellum occurs through xylem and phloem that forms quickly when stimulated by moisture and heat for germination.
The dual functions of storing essential nutrients and digesting stored nutrients in the endosperm contribute the significant growth of roots and shoots as the newly germinating seedling pushes to the surface of the soil.
The bulk of the endosperm is composed of cells with high starch contents and a little zein protein. The starch is composed of two types of molecules, amylose and amylopectin. Amylose consist of unbranched strings of glucose molecules whereas amylopectin molecules are branched strings of glucose units. This molecular structural difference affects the processed food uses of corn starch. Amylose molecules dissolve easier in hot water and do not form a paste whereas amylopectin tends to gel easier. Amylose molecules stain blue in iodine but the amylose molecules do not stain in iodine. Endosperm of most corn varieties will stain blue because of the presence of amylose, although it may only be 25% of the total starch in the endosperm.
The recessive mutant gene waxy (wx) inhibits the production of amylose molecules. This results in production of total amylopectin starch. It is easily identified by the iodine reaction. Being recessive, the gene must be present in both the female and male parent of the hybrid seed, requiring isolation from contamination during increases of parent seed, hybrid seed and grain production. Recessive gene amylose extender (ae) greatly increases the amylose portion of the endosperm starch. This also requires isolation in all steps from seed to grain production to maintain the highest amylose content. Both types of starch affect the final use of the corn grain from animal digestibility to industrial processing. The enzyme amylase will digest amylose and the straight chain component of amylopectin molecules but not the branches.
Three sweet corn genes (sugary, sugary-enhanced, shrunken-2) inhibit or delay the formation of starch in the endosperm. They are used alone and in combination for sweet corn varieties.
The main protein in endosperm cells is zein. It is synthesized in the endoplasmic reticulum of the endosperm cells as amino acids are connected into large molecules. Hardness of the kernel is linked to structure, amount and shape of these molecules. Many mutations have been identified that affect the amino acid content of the zein protein. Recessive gene opague-2(o2) for high-lysine amino acid inclusion in the zein is useful to provide an essential amino acid for animal feed. Unfortunately, it detracts from the hardness of grain. Another mutant called floury-2 (fl2) increases the methionine amino acid component of zein. Both of these genes are recessive and thus requires isolation for purity. Both of these genes do affect kernel hardness and thus can affect processing of grain.
Humans have made corn selections for genes that fit their uses and cultures for a long time. Selections have included endosperm genetics.
Surrounding the starchy endosperm portion of the corn kernel, but within the pericarp is a single (usually) layer of cells known as the aleurone layer. These cells are part of the seed, the result of fusion of one nucleus from the pollen grain with two nuclei from the egg cell in the ovule. Whereas the cells in the rest of the endosperm function mostly to synthesize and accumulate starch, aleurone cells maintain more metabolic activity.
Anthocyanin production occurs within the aleurone cells, resulting in red and purple or blue corn kernels. Genes for lack of anthocyanin in the aleurone, allows the yellow color of starch endosperm cells carotinoid production to show in the common yellow corn kernels. Corn genetics for lack of carotinoid production in starchy endosperm, along with genes for no anthocyanin in aleurone, results in white corn kernels.
Aleurone metabolic activity contributes to much of the seed activity. Phytosterols infuse into the pericarp, contributing to insect and pathogen resistance. Although 80% of the oil in corn kernels is located in the embryo, 12% of the oil located in that thin layer of aleurone cells. Fibers from the aleurone cells and pericarp are processed together as corn bran, the aleurone contributing the oil to the bran animal feed.
The scutellum and aleurone cells are stimulated to produce amylase when moisture and temperatures are appropriate for germination. This enzyme assists in breaking down the starch of the endosperm, and thus making energy available for the growth of the embryo.
This layer of cells is an important component of both the use of corn grain and the growth of the next generation.
Corn pericarp cell walls are composed of polysaccharides, lignin, and protein compounds tightly bound together by another carbon-based chemical called dehydrodferulates (DFA). This is a common feature of many other C4 grasses including cells in leaves and stems. Increases in DFA has been associated with more resistance to ear damage from European, Mediterranean and tropical corn borers and grain storage insects. The feature of tightly binding the cell wall components have been shown to correlate with reduced insect damage in stalk and leaf tissue as well.
Fungi such as Gibberella zeae and Aspergillus species can invade stored grain under some conditions. These fungi not only can destroy grain quality but also can produce mycotoxins dangerous to humans and livestock. The tight binding of pericarp cells can ward off invasion of the grain, but some infection can occur through the silk previous to pollination. There is evidence that higher concentrations of DFA in the pericarp and aleurone is associated with a reduction in mycotoxin production. Apparently, the interaction of the fungal enzymes interacts with the cell walls, causing the release of ferulic acid that is believed to inhibit the ability of the fungus to produce mycotoxins.
The more we learn of the complexities involved in insect and pathogen resistance in corn along with the physical aspects of the corn plant’s structures it is easier to identify with the significance of field tests over multiple environments to select the best hybrid. It is not surprising that the corn genome includes at least 30,000 genes. We also should not be surprised when the ‘best’ hybrid in some environments is not the best in all environments
The kernel is a fruit, the female plant’s ovule outer wall retained as the pericarp. Therefore, the genetics of the pericarp is totally inherited from the female plant. Although the layer surrounding the seed ranges from only a few cells to several cells deep, it has several major contributions to the success of the seed.
Cell walls of the pericarp are thick and tightly held together when the kernel is mature, forming a barrier to the multiple insect and pathogen pests. Genotypes vary in number of cell layers in the pericarp. Moisture loss after black layer is an evaporation processes in which seed moisture must pass through the pericarp, with faster drying linked with thinner pericarps (and loose husk leaves). Thinner pericarp is associated with better digestibility in sweet corn but may be associated with poorer germinating sweet corn. Thicker pericarp is associated with better microwavable popcorn. A thick pericarp has been hypothesized to slow down imbibition during germination resulting in less damage although other factors complicate conclusions. It is probable that pericarp composition has some effect on germination whether from reducing pest damage or imbibition speed. Regardless, the pericarp, essentially a fruit outer wall does have positive and negative effects on our desirable use of the corn kernel.
Pericarp cells in mature kernels are metabolically dead. The lignin of the cell walls is linked to potentially active compounds like phenols that can inhibit fungi such as Fusarium species. Although the genetics of the cells, when alive, was that of the female plant, the layer of cells inside the pericarp is the metabolically-active aleurone. These cells are an actual part of the seed and therefore controlled by the genetics of cross of the male and female plants. Among the products of the aleurone cells are phenols and other compounds for resistance to fungi. These probably move into the pericarp as well. Although the two types of cells can be separated it is probable that proximity can lead to confusion in understanding all of pericarp function.
Recent corn journal blogs have attempted to address some history of corn diseases, including the interactions of the pathogens and the corn plant. Interactions involve the genetics of both the microbe and the host. The list of new, unexpected occurrences in USA and internationally seem to occur every few years. Probably we should not be surprised. As we attempt to improve the hybrids for yield, standability, performance under changing environments we can also inadvertently and unknowingly include genes for susceptibility. Especially vulnerable are genes that allow the recognition of the invader and therefore quick defense response. Furthermore, a corn hybrid that may work well, and not express susceptibility to local pathogens, but when moved to another environment, a pathogen reacts differently.
Microbes also have genes that vary from mutations and sexual recombination. Rapid production of huge numbers of spores, ability to infect multiple hosts often near corn field, and broad, widespread populations of these pathogens is their strength. New variants of the pathogen, adapted to at least a few current hybrids with higher level of pathogenicity, must initially show only in isolated spots in corn fields and easily overlooked. History nearly all ‘new’ races in the USA were not noted until they were widespread. My guess is the genetic variant allowing for the new race (pathotype) was infrequent but present in the pathogen population for some time but was not recognized until damage was common. The more recent occurrence of the bacterial streak of corn, caused by Xanthomonas varicola pv. vasculorum, previously known only in South Africa but within only a few years it was been identified in several US states and Argentina. Was it here for a long time, or distributed by seed or even grain debris? Perhaps it has been a long-time pathogen of other grasses. Or perhaps is a mutant of a related bacterium and we inadvertently selected for susceptibility in corn.
It is doubtful that the battle between new pathogen variants and corn will end. Our best protection must come from careful observations in corn fields and submitting suspicious samples to appropriate specialists for identification. Corn genetic diversity has always allowed selection of resistance, but it does take a few years to implement the hybrid seed production before serious damage to the crop.
Visit us at the ASTA in Chicago, Dec 9-12 (booth G207)
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.