​We generally characterize corn varieties by physical characters that we easily see. Plant height, grain color and hardness, ear height, standability and disease resistance are probably the characters we assume are mostly genetic expression. Each of these characters are mostly directly affected by 1-4 genes. The remaining 30000 genes in every corn plant are producing products not so easily observed but are really the ones affecting final hybrids performance.

The real action influencing everything the corn plant does is occurring in the cells. Not only are the 30000 genes in the cell nucleus on the 10 chromosomes being turned on at appropriate times to produce proteins active in cell metabolism but the DNA and RNA in cell organelles such as chloroplasts, ribosomes and mitochondria are active as well.

The breeding process eventually leading to developing inbred parents for hybrids offers many new combinations of the the genetics. Mutations naturally occurring along the way also contribute to genetic differences not easily detected visually. We may characterize hybrids by obvious features but inside the plant there are differences among hybrids. Although each plant is a single cross hybrid should be genetically identical, Individual plants within a breeding population is not.

It is much similar to the ease with which we classify individual humans by simple visible characters such as skin color or hair color without acknowledging that each individual is genetically different from the next person with same skin or hair color. We have between 20000 and 25000 genes in our chromosomes, and a couple hundred thousand years of genetic mutations within our species and apparently some crossing with related species along the way.

Just as with humans, corn genetics were affected by selection in specific environments. The resulting genetic diversity contributes to new combinations that will drive the future with important adaptations.

Corn Journal has discussed genetics that can be found in the search on Corn Journal page under genetics. One of those blogs from Corn Journal 9/14/2017 follows:

​At least 32000 genes in the ten chromosomes plus the independent DNA of mitochondria and chloroplasts in corn plants. We know the function of relatively few of these genes. We have selected genetics based upon field performance for the traits that we desire for the most part but we don’t know the actual genes involved in establishing grain yield and standability. Certain physiological processes such as photosynthesis can be studies, discerning the enzymes that can be traced back to a genetic code. Based on mutations we can determine the genes involved in endosperm starch formation. Resistance to some diseases can be linked to specific genes.

But how about the genetics that determines number of stomata, allowing for passage of CO2 into the leaves, or loss of water. Do genetics influence the photosynthesis in stomata guard cells determining when they open or close? Chloroplast and mitochondria DNA influence the membrane structure of these organelles. Replication of chloroplasts and mitochondria must involve the interactions of genetics of these organelles with that of the host cells. Movement of minerals into cells and photosynthetic products out is partially determined by cell wall structures as influenced by genetics. Size and number of vascular bundles must be important to movement of water from roots to leaves and ears as well as carbohydrates from leaves to roots and ears.

Genetics influence corn stalk rind thickness, duration of life in pith cells and carbohydrate storage capacity. Root branching, formation of root hairs and ability to absorb water and minerals from the soil are affected by products of the corn plant’s DNA. Kernel number and size also limited by genetics. It is no wonder that corn has a lot of genes.

Many of these genes had to have been established in those Teosinte plants that humans tapped several thousand years ago. Natural occurrence of mutations and human selection of traits expressing adaptation to their environments and desires provide us with large genetic variability. Despite modern molecular techniques to study corn DNA, the complexity of interactions within the corn plants, we are still stuck with our somewhat crude method of field testing in several environments for the best hybrids. We do this with the knowledge that many unknown genes are influencing the final performance and the hope that there remain new genetic combinations that will lead to better performance in the future.

​Membranes dominate the structures in corn cells, being major components of the endoplasmic reticulum, mitochondria and plastids such as chloroplasts.  The nucleus of the cell also includes a double layer of membrane, composed of lipids and proteins.  It functions as a gateway for movement of complex molecules and minerals in and out of the nucleus. As a segment of the chromosome DNA for a gene is activated to produce a RNA code for a protein, the RNA moves to a ribosome to hook the amino acids together forming a protein. Although some of the ribosome action occurs within the nucleus, much happens after the RNA moves through the nuclear membranes into other ribosomes in the cytoplasm. Auxins and other plant hormones interact on the activation of the DNA, requiring regulation through the nuclear membranes.
 
Membranes for each organelle of the cell require very specific proteins, each dictated by the DNA code.  Many of those proteins are coded from the nuclear chromosomes but are also affected by the single chromosomes in mitochondria and chloroplasts. Amino acids with differing nitrogen, hydrogen and oxygen ions arranged around carbon chains determine the composition of proteins and the phosphor-lipids that compose membranes are critical to all cellular function.  Eventual germination of the seed is dependent on formation during seed development and maintenance of membranes during seed storage.

​Poor stands in the field are associated with weather stresses resulting in some seeds not germinating or delayed in germination, resulting in plants much later than adjacent plants. We look at the plant as a whole, but most of the damage is being done at the cellular level. Plant cells are not empty structures but are the vessels where the real action of the plant occurs. Membranes, those long chains of lipids and proteins, not only form barriers to control what enters the cell and its organelles like mitochondria, chloroplasts and ribosomes but also membranes are major components of these structures. These are sites where all of the corn plant’s life must occur. Maintenance of integrity of the membranes within the corn embryo cell membranes is critical to timely germinations.
​
Cell membranes are especially vulnerable to damage during the drying process of the seed and then the expansion after imbibition. They do self-repair, a process requiring both heat energy and supply of carbohydrate energy. Embryos removed from the endosperm will germinate, producing a shoot and root, but adequate heat energy must be supplies and no invasion of pathogens. But they need the stored energy from the endosperm to push through the soil to emerge and receive fresh supply of carbohydrates from photosynthesis.
Cool wet conditions in the field will result in inadequate repair of cell membranes, delaying the emergence of some seedlings. It may be greater with some individual seeds than others because of some seed production and handling conditions or some specific field situations.
More about membranes can be found in the Corn Journal in the search.

We generally think of corn genetic differences as expressed in grain yield and grain characteristics. However, genetics unique to each hybrid influences its reaction to environmental as well as appearance through out the season. Nuclear genes in each cell plus the independent genetics of some cell organelle such as mitochondria and chloroplasts are being expressed in the reactions to environments as well.

​Basic gene function must be effective in all living corn plants except in those few with major mutations. Corn breeders attempt to select individuals that have the characteristics, and thus, the genetics, preferred by the ultimate use of the hybrid. Unseen gene products carry out most physiological functions without our intentional interference. Thousands of genes are regulated and activated for the growth and function of all corn plants without our direct genetic intervention. We do, however, attempt to select those relatively few genes that affect the products most desired by the user of corn. Each of these traits are inherited by relatively few genes.

We can select for flowering timing, relative ear and plant height, grain quality characteristics from the variability present within a breeding population. Resistance to each potential corn disease usually only involves 3-4 genes available in some genetic source within corn. Grain quality characteristics are mostly affected by only a few genes. The challenge is to select for these relatively simple inherited characteristics within the background of those other physiological and morphological functions influence by those thousands of other genes. Furthermore, the expression of those genes must be relative to the varied environments faced by the growing crops.

Added to this breeding difficulty, we must stabilize the genetics by selfing to make inbreds and then match inbreds to make a hybrid combination for repeatable performance in the field. It is no surprise to find appearance differences among hybrids within a variety display plot. Each hybrid exhibited desirable product performance to be commercialized. Each got there by slightly different genetic pathways and because of the necessity of having homozygous parents, each plant within a hybrid will appear identical to each other but different from the other hybrids. Characters such as shape of canopy, length of leaves, and color and shape of tassel are inherited and uniform within a single cross hybrid as the result of uniform homozygosity of the hybrid parents.

Homozygosity of hybrid parents results in uniform and identical genetics for each plant of the hybrid. This applies to each morphological character when the plants are grown in a uniform environment. This applies to corn seedlings as well. PSR has utilized this concept for 33 years assisting seed companies in assuring seed genetic purity of each lot of new seed production. Genetics affect all function and appearance of corn at all development stages.

​We rightfully watch and care about the corn plants as they grow in our fields.  We observe the field as a whole for uniformity of stand and expected growth rate.  We may note some individual plants that are behind others or perhaps show some differences, perhaps with disease symptoms.  We don’t see the individual cells within any of the plants where the real action is occurring.  One of those things was described in this Corn Journal blog written in June 2016.
 
Corn plants now in much of the US corn belt are stretching upwards, for the most part showing little signs of stress.  We have little cognizance, however, of the internal battles that are going on in each of those plants. All plant parts are exposed to potential invaders, through injuries, through stomata or other openings and through direct enzymatic attack from pathogens outside the plants.  Plants have systems to fight the invaders by responding with anti-microbe chemicals or even initiating cell death to limit the damage. 
 
One of the key components of that mechanism is salicylic acid. This chemical was known by Hippocrates about 2400 years ago in an extract from willow bark that could relieve humans with headaches. Yes, it is the main component of aspirin.   Salicylic acid production in plants increases when cells are stressed from pathogens, drought, or toxins.  It functions as a signal molecule, triggering the production of a series of proteins to limit the damage.  Of course, the response time for salicylic acid production and consequential protein production to stop the potential pathogen is dependent on the plant genetics and nutrition.  Pathogens, no slouches in evolution either, often include mutations to slow down the production of salicylic acid by either tying up its component compounds or interfering with the production of the resistance compounds.  It’s a battle out there!
 

​It must be human nature to try to make complex things into simple.  We see this in politics, economics and probably many aspects of human relations seem to want it simple, even if it isn’t.  Those of us that have studied corn and its diseases and certainly anyone growing a corn crop know that the actual environmental interactions with the crop is complex but we still are inclined to try to simplify the interaction between a microbe and the corn plant.
 
In reality, corn roots are invaded by a variety of fungi and bacteria, some of which simply live off of plant products and don’t cause any visible harm to the plants.  Some would call these organisms as endophytes (living with plants but not causing damage). 
 
Presence of these may be detected by the host plant, causing it to produce compounds that restrict the growth of these endophytes into more active plant cells.  In some cases, this appears to restrict more active pathogens.  Species of the genus Trichoderma have been noted as a type of biological control, but also some studies have noted fungal species of Fusarium, Acremonium, Aspergillus, and Botryodiplodia have similar interactions with corn.
 
It becomes more difficult to classify organisms that may once be a harmless endophyte but later, perhaps as the plant begins senescence either because of age, stress or simply shortage of adequate products of photosynthesis in some tissues. Cells in these areas perhaps cannot produce the resistance products needed to stop the foreign organism from killing weakened host tissue.  Do we now designate the organism as a pathogen? 
 
Often it is easier to name a disease, implying that an aggressive pathogen attacked the plant is appealing.  Often, however, looking at the more complex aspects that allowed the organism to attack the plant could help avoid the repeat in the future.  With many plant physiology, environmental and micro-organisms dynamics it is difficult for research as well as to adequately and completely describe.

​Major growth regulation in corn is done with hormones.  There are three major types: cytokinins, auxins, and gibberellins.  Each has specific functions in the metabolism and growth of the corn plant. 
 
Cytokinins, originally produced in the corn seed scutellum, migrate to the root tip where they stimulate cell division.  Later, cytokinins trigger the cell division in all the growing points of the corn plant. These include the lateral root tips, the stem meristem and each of the lateral stem buds, including the one (or more) that becomes the ear.  Cytokinins also are active in delaying senescence of leaf tissue. Zeatin is a common cytokinin in corn and other plants.
 
Auxins influence cell elongation, stimulating it in stem cells but inhibiting it in root cells.  Auxins inhibit elongation of lateral buds countering the cytokinin effect of cell division.  It is the balance of the two hormones that affects corn plants tendency to tiller. The most common auxin is indole-3-acetic acid (IAA). Apical dominance in plants is controlled by this auxin.  This auxin also influences flowering and inhibition of abscission layers at the base of leaves and maturing kernels. Herbicides such as 2,4-D and dicamba are auxins that disrupt plant growth and development.
 
Gibberellins include more than 100 compounds that effect shoot elongation, seed germination and maturation of grain. These hormones are produced in root and stem meristems as well as tips of new leaves and seed embryos. Gibberellic acid is the most common compound that can be artificially added to plants.   Gibberellins tend to delay  kernel maturation and are effective in determining plant height.
 
Synthesis of these hormones is determined by genes, of course.  Plant height of different varieties involves these genes as the hormone synthesis involves several steps, with a few major genes causing dwarfness, and multiple genes affecting slight differences in plant height. Nearly all aspects of corn plant growth is affected by hormones.
 
Soil microbes also produce auxins and cytokinins that can affect root development and ultimately affect phosphorus uptake by changing the balance of hormones in roots.  Potential microbial seed treatments attempt to use these interactions to stimulate early corn growth.
 

​Corn is just emerging from soil in some fields but is approaching V6 in others.  The seedlings have been fighting seedling pathogens, but the more developed plants now must battle the leaf disease pathogens causing northern leaf Blight, southern leaf blight and gray leaf spot.  This involves genetics of the corn plant and of the pathogen. Corn Journal summarized this battle in 6/30/2016.
 
The chemical warfare between the host plant and pathogen occurs without much of our attention.  Differences in resistance to different pathogens among corn hybrids can be visible and we attempt to characterize these differences, but the cellular interactions have required careful lab studies.  Plants preserve energy by delaying the pathogen defense until the pathogen has invaded.  With fungi, the initial reaction is to a common component of nearly all fungal cell walls (chitin).   With that detection, signal hormones, such as salicylic acid is produced.  The fungus produces enzymes to attack the host cells, as the signal hormones activate the resistance genes to produce the proteins to limit the fungus.
 
Most corn pathogens feed on the dead cell tissue, even after the progress of the pathogen in the leaf tissue is stopped.  From the limited, dead tissue the fungus produces spores and spreads to fresh leaf tissue on the same or different plants.
 
A few corn pathogens, however, can only reproduce when feeding on living cells.  Smuts and rusts are these sort of pathogens that are called biotrophs.  These fungi invade living cells without killing the cells, while feeding on the cell and then spreading to adjacent living cells.  Resistance to this type of pathogen can involve a single gene system in which the host plant detects the presence of this type of pathogen and then produces the signal molecule at such concentrations that the host cell dies and, consequently, so does the pathogen, stopping the spread of the pathogen to adjacent cells.  This resistance system is generally inherited by a single gene so genetic diversity in the fungal population often includes single gene mutant variants (races) that overcome this sort of resistance system.  Common smut fungus (Ustilago maydis) includes a race that produces an enzyme that digests the signal molecule salicylic acid before it can cause the host cell to die and therefore the fungus now can spread to adjacent cells. Single gene resistance to rusts for many crops, including corn, are commonly overcome by single gene differences in the rust pathogen that suddenly makes a variety susceptible. Genetic diversity works for both parties.
 

​This wet late spring has resulted in pools of water in low areas of Midwest US fields.  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 forgiving this pathogen for forming these unusual corn structures in a few spots of the field.  In addition, it is just part of the interesting biology of corn.