I recall a phrase used by the plant physiology professor in a lecture that he used to make a point.  While traveling through mountains, he was arguing with his wife as to whether they were going up hill or down, confused by surrounding terrain. He claimed he got of the car and poured water on the road to see which way the water flowed.  Then, he made the point to the students “water runs downhill!”.
 
Moisture from soil moves into the drier tissue of the planted dry corn seed. This imbibition causes the membranes of cells and their contents to expand, sometimes damaging the membranes.  Cellular membranes have the ability to self-repair, but this process occurs more quickly with heat energy. Fast movement into the seed under cold soil conditions can cause significant damage to cell function ultimately resulting in slow or no germination.
 
Movement of water into the seed is slowed by the outer layer of cells in the pericarp. Breakage of this layer, results in more rapid uptake of water by the seed, potentially inhibiting seed germination. Seed treatments include a polymer coating to slow the uptake speed of water into the seed, allowing for membrane repair even when planted in cooler conditions. 
 
Small breaks to the outer layer of cells in corn seed is practically unavoidable during the movement of harvested seed, despite extreme care of the seed producer.  Ultimate uniform and nearly complete germination of the seed is enhanced by polymers applied to the seed outer layer.  The warm germination test distinguishes seed sufficiently injured that it cannot recover but the cold test identifies seed that cannot recover under the usual cooler soils conditions common for temperate zone corn planting.  Pericarp cells, derived from the female plant, have some influence affecting the speed of water imbibition.  Coating of the pericarp with a polymer can slow the imbibition process and resulting in less membrane damage. 
 
Imbibition does not require living cells but simply the physical act of water moving down hill.

​Storage of seed requires very slow metabolic activity, enough to keep membranes, but not enough to cause premature death of the embryo.  Low seed moisture is mostly responsible for maintaining life in this semi-dormant condition.  After planting, however, we want the seed to imbibe enough water to stimulate more activity.  This process of imbibition was addressed in Corn Journal blog of 4/4/2017.
 
As the corn kernel is developing after pollination, embryo shoot and root cells are formed in a way that could quickly germinate with the moisture present in the tissue.  A temporary dormancy prevents this from happening.  Removal of the milky endosperm from the embryo as early as 10 days after pollination will allow the growth of root and shoots.  Abscisic acid (ABA) in the endosperm appears to be the hormone involved in avoiding germination in seed before the full development. At least 10 single gene mutants are known to overcome dormancy in developing maize seeds, resulting in germination while on the ear (vipipary).  Drying of the kernels initially by displacement with starch formation and then by air inactivates the dormancy.
 
Imbibition is the movement of water into the seed.  It is a physical phenomenon, independent of the germination quality of the seed and of temperature.  Movement of water into the seed is relatively fast, most occurring within a few hours. There is some evidence that slowing the imbibition by some seed treatments reduces the harm to membranes by giving them more time to repair.  Rehydration of cellular tissue and chemicals cause swelling.  Membranes, shrunken by drying, strengthen and activate but some solutes escape before damage from the drying is repaired.  As the mitochondria are activated, ribosomes begin producing proteins needed for more cell growth, starches from endosperm are digested to form glucose molecules to be transported to the mitochondria in embryo cells.  Oxygen uptake into the seed increases rapidly during imbibition - an indication of the active respiration occurring in cells.  Heat, moisture and oxygen availability influence the speed in which imbibition initiates the germination of the corn seed.
 
Humans, without knowing cellular physiology, selected for these traits for Zea mays.  And we get the benefit. 

 ​Dry corn seed are alive and breathing.  Respiration in the seed, like in the rest of us, occurs in the mitochondria of the cell.  The process of breaking down sugar provides the energy for creation of enzymes needed to maintain membrane structures in the seed that will be needed when germination begins.  
 
Membrane deterioration increases as the temperature and moisture increase.   These interactions of storage temperature and moistures have been shown to have a drastic affect on eventual germination percent of stored seed.  Even size of root and shoot length of the seedlings is reduced if the seed was stored under conditions of higher humidity and temperatures. 
 
Membranes not only surround individual cells but also the main sites of activities in cell organelles. Enzyme activity along these are the sites of protein production in ribosomes, transfer of proteins and other products are often done via cellular membranes.  Much of this activity is guided by DNA within the cell nucleus, its integrity and activity affected by the nuclear membrane.  Because natural breakdown of membranes increases with temperature and moisture, the need for higher respiration rate increases when seed is stored under poor environments.  Seed stored at 9% moisture content and 10°C (50°F) retained nearly 100% germination for 4 years whereas the same lot of seed stored at 15% moisture content and uncontrolled temperatures as high as 38°C (100°F) had o% germinations.  Reducing the seed moisture percent to 11% even under the warm conditions increased the percent germination to 90% (Plant Physiol. (1967) 42, 1071-1076).  Many seed studies and experiences since then have verified the principle that drying seed and storing under low temperatures are essential to maintaining eventual high percentage germination of corn seed.

​The pericarp surrounds the whole corn kernel, affecting the insect and pathogen invasion of the kernel and water penetration in the kernel.  It may be 2-20 cells thick and is, genetically, female tissue.  It is also without pigments.
 
​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. Although only a single layer of cells, it can include 30% of the total proteins of the endosperm.
 
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 carotenoid production to show in the common yellow corn kernels. Corn genetics for lack of carotenoid 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.

​This thin outer layer of the kernel, originating from the female plant becomes an important contributor to ability to fend off pathogens and insects searching for the carbohydrates stored in the endosperm of the enclosed seed.
 
Maize Weevil (Sitophilus zeamais), showed that the cross-linked structural components of the pericarp cell walls were highly correlated with resistance to this insect.  Other factors included phenols (Afr. Crop Sci. J. 9:431–440) produced by the pericarp cell metabolism and even endosperm hardness (flintiness) contributed to reduced susceptibility to this storage insect (Crop Sci. 44:1546–1552 (2004)).

Pericarp tissue also is a barrier to entrance into the seed by multiple kernel rotting fungi.  Most enter the ovary through the silk channel immediately before pollination.  This becomes most evident when silks are left exposed for several days in an environment favoring the pathogen.  After invasion, the fungus can spread cell-to-cell within the pericarp through small holes (pits) in the cell walls that allows movement of metabolites between cells.  Integrity of the pericarp is a significant factor in avoiding invasion by many potential fungal species.

The phenomenon known as silk-cut can expose the seed to fungal infection.  After the pollen tube grows down the silk channel and dumps the pollen nuclei into the ovule, silk tissue deteriorates and detaches from the ovary.  Not all silks are pollenated even under ideal conditions, leaving some attached to their ovary while adjacent pollenated ovaries grow.  These remaining silks interfere with normal contiguous growth of the pericarp cells in the adjacent ovary wall (Plant Disease 81 (5):439-444).  This can result in a break in pericarp as the kernels enlarge and thus an opening for invasion by fungi.  Genetics and environments influence the occurrence of silk-cut.  Stresses that delay silking beyond pollen availability can be an important factor but genotypes vary in vulnerability both to reaction to the stress and probably the tendency of this phenomenon.
 
The pericarp, being completely dependent of the female plant genetics, adds to the significance of the hybrid seed producer’s decision of which parent inbred to use as the female.  Both parents contribute to the hybrid ‘vigor’ but the female parent determines the pericarp characteristics.

 ​The fact is a corn kernel is a fruit, composed of a part of the female plant, the thin outer wall, and the remaining from fertilization of the female egg by the male sperm nuclei.  The cells in the resulting embryo include organelles such as mitochondria that are duplications of those from the female plant as the male’s contribution is only half of the resulting DNA in the seed.  Mitochondria genetics, as inherited from the mother plant, may have subtle affects on the hybrid plant but could be major in seed aging and germination.
 
The powerhouse of almost all living cells in all plants and animals is a very small, bacteria-like organelle called a mitochondrion. It is similar to bacteria in its size, shape of chromosome, organization of its DNA and function.  Mitochondria presence in all from the smallest of single cell animals and plants to the largest has led to the hypothesis that it originated as symbiotic relationship with a bacterium 3 billion years ago.  The clear advantage of having this organelle that could transform carbohydrates into chemical forms of energy that allowed production of proteins for growth and movement of muscles in animals is overwhelming. 
 
Mitochondria are the size of bacteria and therefore visible only with a strong light microscope magnifying at 1000X but the details require electron microscope power at 30000-50000X.  With this extreme level of magnification, mitochondria are shown to be composed of a surrounding double layer of membranes enclosing many folds of membranes.  Membranes are significant to function in that these are the sites in which the enzymatic action allowing the energy holding the glucose molecule together is released and combined with nitrogen and phosphorus into another chemical compound, Adenosine triphosphate (ATP). This compound released through the membranes into the rest of the cell for normal cell metabolism.  It is also the site in which CO2 is released during respiration.
 
The fact that mitochondria have their own DNA has had dramatic affects on corn.  Individual cells may contain from a few to hundreds of mitochondria and they replicate on their own, independent of nuclear chromosomes.  However, when sexual reproduction occurs in plants or animals, and the nucleus from the male donor fuses with the nucleus of the female egg cell, no mitochondria are passed along.  Consequently, the mitochondria in the progeny are only those from the female parent.  Although the size and genetics of the nuclear DNA is overwhelmingly greater than that of the mitochondrial DNA, and the most profound genetics remains with the nucleus, mitochondria inheritance has had some dramatic affects on plants and animals, including us humans.
 
Amazing how we are so dependent upon such small things like mitochondria!
 

 ​​The corn kernel is a fruit with one giant seed.  We humans mostly bred and selected this grain for its use as a food source, increasing the endosperm size with carbohydrates.  Selecting for desirable seed traits has been at least somewhat secondary to the grain production.  On the other hand, uniform and reliable field emergence is a major contributor to corn grain production in modern corn hybrids.  This is dependent on the science and experience of seed producers.
 
Much of the propensity for high germination is dependent upon the female seed parent.  Pericarp, being totally part of the female plant, affects rate of moisture loss during drying, vulnerability to physical damage from handling of the seed and susceptibility to ear molds.  Mitochondria genetics are totally inherited from the female parent.  Much of the damage from rapid, cold imbibition of water at the initial stage of germination involves the mitochondrial membranes.
 
Maize kernels handled as grain need to be stored at 15% moisture to avoid mold.  Modern hybrids are usually allowed to dry in the field well beyond the 30-32% moisture level that black layer forms and completion of movement of carbohydrates to the kernel.  It is usually most economic to allow drying in the field before finishing with artificially drying.
 
Most maize seed begin losing germination capacity if left in the field during those final days of slow drying in the field.  Studies have shown that greater germination percentages are retained if seed is harvested in the 35-40% moisture level and then is quickly dried with lots of air and less than 100°F.  Retaining the higher moisture level for some time initiates metabolism in the embryo, essentially an artificial aging process.  Seed dried to about 12% moisture is considered optimum of storage and retention of high germination rates.
 
Producing and retaining high germination is the result of research of each hybrid parent’s vulnerability as well as experience with weather and facility.  Drought damage during grain fill, rain delaying harvest, drying at too high temperature and not enough air, rough handling during processing and adding too much water during seed treatment can contribute to below standard germination.  One can write a manual for production of seed corn but ultimately it takes some experience to apply the science.  Like most agriculture. 

​​Leaf epidermal cells walls and the waxy leaf surface provide the first line of defense against microbes.  Pathogens adapted to overcoming this defense set off the next defense system after penetrating the leaf.  This is initiated by the plant detecting the presence of the intruder. Plant cells nearby detect the presence of a protein exuded by the pathogen. Such proteins are called effectors, as they are detected chemically by host cells near the invader.  Upon detection, these adjacent host cells produce potential microbe-inhibiting compounds such as reactive oxygen, nitric oxide, specific enzymes, salicylic acid and other hormones to effectively thwart the pathogen growth.  Much initial reaction is limited to host cells adjacent to the infection site.
 
Resistance to corn leaf pathogens such as Exserohilum turcicum, cause of northern leaf blight, Cercospora zeae-maydis (gray leaf spot) and Bipolaris maydis (southern corn leaf blight)
Involve detection of that specific pathogen and production of more general antimicrobial products in the immediate area of the pathogen.  These two steps are inherited independently. Perhaps the pathogen detection system is more specific to the pathogen, accounting for a corn variety being more resistant to one pathogen than another.  On the other hand, I am suspicious that if two pathogens arrive in the same area of the plant, only one will survive, as if the plant reacts to the first one by producing general resistance compound that inhibit the infection by the second one to arrive in the same area.
 
The system described above is referred to as general or horizontal resistance.  It is controlled by 3-5 genes for products to detect and reduce spread of the pathogen.  Horizontal resistance is expressed in corn plants by fewer leaf disease lesions.  Evaluation of varieties for this type of lesion has some ambiguity however, because the number of lesions or amount of leaf damage is also affected by the intensity of disease pressure.  Heavily diseased leaves from the previous season in fields of low tillage, with frequent early season rain can result in more leaf lesions in a variety of good general resistance to a pathogen than will occur in one of poor resistance with little disease pressure.
 
Characterization of horizontal resistance level to a pathogen requires a rating scale that has some consideration of disease pressure and relativity to other varieties.  It is best done when each variety is exposed to the same pathogen intensity at the same stage of leaf maturity. Differences expressed as lesion numbers, size of lesions and percent of leaf destruction can be used to indicate the level of general resistance to that pathogen.  I prefer to make ratings based upon several plants exposed to the pathogen in what I project to be somewhat heavy disease pressure in most USA corn environments.  With artificial exposure to the pathogen by placing spores in the plant whorl, each plant receives more-or-less the same pressure.  Expression of resistance will show 1-2 weeks later.  Those varieties with abundance of larger lesions are deemed more susceptible than those with fewer and often smaller lesions.  Consequently, it is assumed that will simulate the reactions in fields with somewhat heavy pressure from that pathogen.
 
Any evaluation of horizontal resistance includes consideration of disease pressure and relativity to other varieties. From Corn Journal 7/11/2017.

Virus genetics are very simple. They penetrate the genetically complex host cells, utilize the hosts metabolism to duplicate themselves and move on to another host cell.  COVID 19 virus has 15 genes in its RNA.  Humans have about 20000 genes in its nuclear chromosomes plus independent genes in some cell organelles such as mitochondria.   Corn has about 40000 genes in its chromosomal DNA plus genes in chloroplasts and mitochondria.  The human selected genes that allowed the development of modern corn from its Teosinte origin only involves 2-4 percent of the total genes in present corn varieties.
 
One marvels at the complexity of the interactions that are occurring within each cell of a corn plant as it not only absorbs light energy, translates it into metabolic energy for sustain growth and more metabolism.  Meanwhile the corn plant is fending off potential invaders of insects and pathogens.  Mutations in genetics of those invaders can overcome the simple detection method of the host that triggers the corn plant to produce metabolites to stop the pathogen.  Human selection of more stable resistant corn has resulted in resistance inherited by several genes. Usually, 3-5 genes are involved in limiting a pathogen success in a corn variety.  Occasionally a single gene in corn is effective but often only for a short time.  The Ht1 gene for stopping Helminthosporium (Bipolaris) turcicum was useful in USA in late 1960s for about 15 years but eventually the mutants in the fungus produced metabolites escaping the Ht1 gene’s products, making use of the gene no longer effective.  
 
Adaptability of corn to multiple environments is due to the large genetic resource among those 40000 genes.  Corn being an annual plant, separation of male and female flowers and abundant genes for selection has allow humans to desirable traits.  Mutations and new mixes of genes from different backgrounds has allowed these selections to continue the increase in grain production by this plant.  Research in the nature of the corn genetics continues as molecular methods discern more about corn genes.  One article summarizing current status of corn genes can be found at https://www.cell.com/plant-communications/pdf/S2590-3462(19)30010-0.pdf.

​At the same time that the complexity stimulates the research interest for some to explore with their  molecular research, the simple pollination of the corn species, and more complex testing for desirable hybrids by those making selections for current environments has allowed participation of a large number of humans in improving this crop.

 The genetic code of all living things exists as a long string of 4 nucleotides adenine, thymine, guanine and cytosine.  We abbreviate as A, T, G and C.  Each nucleotide is composed of a phosphate, a sugar and a nitrogen base.  They slight differences in their composition that affects their chemical behavior.  RNA and DNA differ by the sugar, ribose for RNA and deoxyribose for DNA.  A gene is composed of a chain of these nucleotides interpreted as sets of three after the start sequence is established.  Each set eventually gets translated to produce an amino acid when moved to the cellular ribosome where the amino acids are linked to form proteins. These proteins often become the enzymes needed to carry out the metabolism of the organism.  Enzymatic function is often affected by the sequence of the amino acids within the proteins.  Exact duplication of the DNA is required for each nucleotide sequence to result exact duplication of the protein and expected function in some metabolic process.
 
Some of the ‘errors’ made in the RNA or DNA result in meaningless mutations and some allow the natural and human-driven selection of variability for choice corn varieties.  Of course, the diversity mechanism is active in all things with RNA and DNA, resulting in changes in some pathogens of corn as well.  The opportunity for change gives reasons to appreciate beneficial 
variability as well as to be alert for those from which we do not benefit.
 
Corn Journal blog of 7/27/2017 addressed one of those dramatic events affecting corn.
 
​All living cells of plants and animals have mitochondria, organelles that convert carbohydrates into the useful form of energy that drives synthesis of metabolites in cells.  Mitochondria are believed to be descendants of bacteria that became symbiotic with cells in the early evolution of most living forms.  They retained their own DNA, are transferred to the next generation only in eggs cell and not sperm. They replicate within cells but the host cells have some control on the rate of replication.  Energy conversion in mitochondria occurs on their folded membranes in a series of chemical reactions.  Regions of the plant undergoing rapid cell duplication have more mitochondria.  This includes the tassel cells of a corn plant.  The pollen mother cells in that region undergo meiosis and duplication, driven partly by the energy conversion by concentration of mitochondria in those mother cells.
 
A small defect in mitochondrial DNA of an inbred caused a defective membrane product in those mitochondria resulting in incomplete development of pollen.  This was found in a corn breeding program in Texas.  As the inheritance of this condition was known to be only transmitted independent of nuclear DNA, it was called Texas male sterile cytoplasm.  It became a useful tool to corn hybrid seed production because it was easily transferred in breeding programs to the female parent of a hybrid, and thus avoiding manual removal of tassels in seed production fields. Use of T male-sterile cytoplasm became common in the worldwide corn in the 1960’s.
 
It was noted in the Philippines in 1961, that a fungal pathogen, then known as Helminthosporium maydis, was especially aggressive on several hybrids with T cytoplasm. Despite a few scattered reports elsewhere it was not until 1969 that the connection between increased occurrence of this disease and T cytoplasm became alarming.  Majority of seed produced for 1970 corn season had T cytoplasm, the main exceptions being new hybrids in which the conversion to sterility of the female parents was incomplete.
 
Although the pathogen was normally found in the southern half of the corn belt, and adequately controlled by products of nuclear DNA genes, this disease was found highly destructive in northern corn belt areas as well. A race of the fungus (now named Bipolaris maydis and by its sexual stage Cochliobolus heterostrophus) called race T, produces a toxin that causes death to cells with mitochondria having the DNA with the defect associated with T male sterility.  All cells of the corn plant with these defective mitochondria were vulnerable to the fungus.  This included the cells in developing seed resulting in diseased stored grain as well as overwintering leaves and stalks.  Normal resistance mechanisms to the pathogen were ineffective because the toxin destroyed these defective mitochondria.
 
As the relationship with T cytoplasm was realized, seed companies worked to change, and within a few years, the disease subsided back to its normal distribution.  It was a new learning experience of interaction of corn and pathogen biology.

​Humans are now faced with mutations in the coronavirus that is causing drastic illness.  Mutations in DNA and RNA occurs continuously with benefits and detriments to humans and other forms of life.  It is the cause of diversity we see and don’t see in our daily lives.
 
About 9000 years ago, give or take 1000 years, people in Southern Mexico were finding ways of using seeds of a weed we now call Teosinte as food.  It was inefficient in that the seed were encased in a hard fruit wall and that these fruit (grain), were easily shattered from the thin rachis, spreading the seed for the next generation. The hard encasement (fruit wall) allowed the next generation to pass through the gut of a bird, causing in spread of the species.  These tall grassy, tillered weeds had many flowers per plants and flower structures that encouraged cross-pollination.  It was about the time in human history that our species started to switch from being food gathers to farming.  Archaeologists now have evidence that about 4500 yrs. ago, farmers in southern Mexico had identified and cultivated a variant of Teosinte that had a cob with seed encased in a thin fruit wall (pericarp) that allowed easier preparation for food.  We now know that it only took a few major gene mutations to change this plant to one that had a thin pericarp, a rachis to a cob and a drastic increase in number of kernels from the 8-12 on the original weed to 20-50.  From that beginning, the new type was gradually spread throughout North and South America.  As humans moved it to new environments and selected those that best survived and had characteristics best for them as a food source, corn became a mix of local adaptation and maintaining some of its wild Teosinte past.  By the time of Columbus arriving in the New World, corn was cultivated from Canada to Argentina, from hot humid tropics to dry areas of western US and Argentina. 
 
Selections made by locals had resistance to local corn diseases and insects, soft kernels for easy flour production, hard kernels for better storage, different kernel colors for local preference, fewer ears per plant for easier hand harvest and many other characters that came along with diverse local needs. There were varieties that rapidly expanded endosperm when heated (popcorn) and those with an enzyme delayed sugars to be converted to starch (sweet corn). After Europeans introduced this wonderful crop to the other continents, selection to each of those environments further allowed selection for adaptation.  Consequently, corn genetics is more diverse than any other crop, always available for the next request that we humans can make from it.
 
As humans (corn breeders are usually human! LOL) select corn genetics best fitting to their purpose, and attempt fight destructive pathogens and insects, beneficial mutations are being chosen.  No reason to think this will not continue as good and bad mutations occur.

​Energy for creating resistance to a pathogen is wasted if the pathogen is not present.  Corn, like most plants and animals, gains efficiency by keeping the genetic codes for creating resistance in the DNA in cell nucleus.  Signaling proteins in the cytoplasm of cells are apparently specific for each need such as creation of cytoplasmic resistance to an invading pathogen. Small RNA molecules cause string of DNA in the nucleus to create Messenger RNA that migrates through the nuclear membrane to ribosomes within the cell.  The RNA codes for distinct strings of amino acids, creating the specific proteins needed for creating the resistance to the invading pathogen. The speed and intensity of these elements contribute to the effectiveness of the resistance.  We attempt to measure this effectiveness with our field evaluations of a plant reactions to the pathogen by rating overall lesion development and just assume that the signaling, DNA transcription, mRNA movement and protein creation happened.  We cannot avoid marveling at the efficiency of activity in living cells. 

​We are witnessing a wide range among human’s ability to fight off the coronavirus causing the 2020 pandemic.  The dynamics involved in these differences are not much different than corn’s reaction to pathogens.  Following is a blog discussion of horizontal disease resistance in corn from Corn Journal of 7/11/2017.
 
Leaf epidermal cells walls and the waxy leaf surface provide the first line of defense against microbes.  Pathogens adapted to overcoming this defense set off the next defense system after penetrating the leaf.  This is initiated by the plant detecting the presence of the intruder.  Plant cells nearby detect the presence of a protein exuded by the pathogen.  Such proteins are called effectors, as they are detected chemically by host cells near the invader.  Upon detection, these adjacent host cells produce potential microbe-inhibiting compounds such as reactive oxygen, nitric oxide, specific enzymes, salicylic acid and other hormones to effectively thwart the pathogen growth.  Much initial reaction is limited to host cells adjacent to the infection site.
 
Resistance to corn leaf pathogens such as Exserohilum turcicum, cause of northern leaf blight, Cercospora zeae-maydis (gray leaf spot) and Bipolaris maydis (southern corn leaf blight) involve detection of that specific pathogen and production of more general antimicrobial products in the immediate area of the pathogen.  These two steps are inherited independently.  Perhaps the pathogen detection system is more specific to the pathogen, accounting for a corn variety being more resistant to one pathogen than another.  On the other hand, I am suspicious that if two pathogens arrive in the same area of the plant, only one will survive, as if the plant reacts to the first one by producing general resistance compound that inhibit the infection by the second one to arrive in the same area.
 
The system described above is referred to as general or horizontal resistance.  It is controlled by 3-5 genes for products to detect and reduce spread of the pathogen.  Horizontal resistance is expressed in corn plants by fewer leaf disease lesions.  Evaluation of varieties for this type of lesion has some ambiguity however, because the number of lesions or amount of leaf damage is also affected by the intensity of disease pressure.  Heavily diseased leaves from the previous season in fields of low tillage, with frequent early season rain can result in more leaf lesions in a variety of good general resistance to a pathogen than will occur in one of poor resistance with little disease pressure.
 
Characterization of horizontal resistance level to a pathogen requires a rating scale that has some consideration of disease pressure and relativity to other varieties.  It is best done when each variety is exposed to the same pathogen intensity at the same stage of leaf maturity.  Differences expressed as lesion numbers, size of lesions and percent of leaf destruction can be used to indicate the level of general resistance to that pathogen.  I prefer to make ratings based upon several plants exposed to the pathogen in what I project to be somewhat heavy disease pressure in most USA corn environments.  With artificial exposure to the pathogen by placing spores in the plant whorl, each plant receives more-or-less the same pressure (www.psrcorn.com/pathology.html).  Expression of resistance will show 1-2 weeks later.  Those varieties with abundance of larger lesions are deemed more susceptible than those with fewer and often smaller lesions.  Consequently, it is assumed that will simulate the reactions in fields with somewhat heavy pressure from that pathogen. 
 
Any evaluation of horizontal resistance includes consideration of disease pressure and relativity to other varieties.

 ​Humans and plants have similarities in fighting pathogens. Structural characters such as skin on animals and tight epidermal cells on plant leaves prevent invasion by most micro-organisms capable of destroying internal tissues rich in nutrition for them.  But evolution favors some organisms able to avoid this outer defense system, requiring the host to detect their presence and turn on resistance systems.
 
Corn leaf epidermal cells are tightly connected except for the stomata. The vast majority of microbes surrounding corn plants cannot penetrate the plants. The few that do have the capability, perhaps by enzymatically drilling through the epidermal cells to enter the leaf tissue, set off the alarm. In some cases, the plant’s first response is increasing the production of salicylic acid in the area of the invasion. This turns on the genes for production of the protein, often an enzyme, with the capacity of stopping the pathogen from spreading.  This final product may be effective against several potential pathogens or specific to one species.
 
 
​There are genetics, of course, behind the chemical responses to attacks by pathogens.  The genetics must relate to detection of an attack, perhaps detection of the specific pathogen, production of a general or specific anti-pathogen material and speed of the response.
 
Although all resistance to corn diseases involves multiple genes affecting the biology for the processes mentioned above, in many diseases there is a single corn gene that has a drastic, critical affect on the pathogen.  This is called qualitative resistance.  In the case of rust diseases, the pathogen is killed almost as quickly as it invades a cell.  With Exserohilum turcicum the plant with an Ht gene stops the fungus as it enters the vascular system, inhibiting the fungus from producing usual northern leaf blight lesions and spores to further spread the disease.  Qualitative resistance is convenient for the corn breeder to select during the breeding process but, unfortunately, nearly always the population of the pathogen includes individuals with a single gene that produces a product to overcome the resistance product.  Eventually, natural selection results in increasing presence of those pathogens with this gene and the the corn single gene is less useful.
 
The more stable resistance involves strengthening the detection, and the speed and concentration of the anti-pathogen materials.  This is called quantitative resistance. It is controlled by several genes and therefore more difficult to identify by breeders.  It is usually reflected by fewer and smaller lesions but assurance of exposure to the pathogen comparable to potential for the commercial life of the hybrid is not simple.  Most diseases are heavily influenced by environments which vary by location and season.  Most susceptible genetics are eliminated in breeding nurseries, but we do get surprised occasionally either with increased intensity of a disease or new pathogen changes. 

​Humans are witnessing the affects of genetics of a virus affecting human behavior everywhere.  Dynamics of the COVID-19 and people interactions will have some permanent affects, some of which are not yet clear.  Biology, affected by genetics, in plants and their pathogens have similar long-term interactions.  We witnessed this in the outbreak of the Southern Corn Leaf Blight in 1969 and 1970.  That phenomenon was blogged in Corn Journal issue 129/2019.
 
Race t of Helminthosporium maydis(Bipolaris maydis) (Cochliobolus heterostrophus) spread across most corn growing areas in USA and elsewhere in 1970.  The traditional version, race 0, of this pathogen was common in the Southeastern USA where temperatures and humidity favored the biology of the fungus.  A related fungus Helminthosporium carbonum (Bipolaris zeicola) (Cochliobolus carbonum) was a common pathogen of corn but tended to be more frequent in the northern part of the US corn belt.  The summer of 1970 not only featured epidemics of race T of H. maydis but spread of this pathogen to much of northern corn belt. This allowed the co-mingling of the two species.
 
The two species were distinguished by microscopic examination of their conidia, the asexually produced spores associated with spread of these fungi.  H. maydis spores were consistently curved and appeared to be gray when viewed with a light microscope.  H. carbonum conidia were darker in pigment and mostly straight.  Both species had shown to have similar sexual reproduction structures and to have distinct sexual mating types.
 
Seed companies, including the one that I had just joined, were checking their inbreds and hybrids in the summer of 1972 to make sure there was no remnant susceptibility left among their materials. I was surprised to find a wide range of shapes and sizes of lesions naturally occurring among materials that looked like southern corn leaf blight in our central Illinois nursery.  Examining the spores under microscope showed a range of spore shapes intermediate to H. maydis and H. carbonum.  Other pathologists found the same thing.  It had been shown previously that these two species could cross in lab experiments and now it appeared that the wide-spread distribution of H. maydis into regions where H. carbonum was common allowed multiple opportunities for sexual crosses between the two.  This apparently accounted for the range of conidia morphology seen in the summer of 1972. 
 
The resulting population of these multiple crosses further sorted in virulence on corn.  H. carbonum already had been found, with one race (race 1) to produce a toxin affecting a few inbreds homozygous recessive to the toxin. Another group of this pathogen appeared to mildly pathogenic on corn leaves was defined as Race 2.  After 1972, some inbreds and hybrids were found to be susceptible to Race 3, resulting in distinctive long, narrow lesions. In 1980, inbreds with B73 backgrounds, commonly used as female parents in seed production fields, were infected with a distinct race 4 of H. carbonum.  Apparently, the crosses of the two related fungal species resulted in new genetic combinations.
 
This event occurring 50 years ago not only changed corn breeders wariness of corn’s disease vulnerability but also all involved with corn to be constantly observing for subtle changes in pathogen-host problems.  Biology of one affects biology of others.
 
 

​Corn nucleus includes 30000-40000 genes in its chromosomes. These 10 chromosomes are sorted and combined with the chromosomes of the other parent during pollination, both parents contributing to the hybrid.  Cell organelles, such as plastids and mitochondria, have up to 100 genes in each small structure but these are not contributed by both parents during pollination. All organelle DNA is contributed by the egg cell. 
 
Small mutations in the in mitochondria of the female parent can result in drastic affects on the plant.  Such mutations resulted in cytoplasmic male sterility in CMS corn because in reduced the energy within pollen producing cells to make fertile pollen. This happens in T, C and S male sterility.  Mitochondria function however is not completely dependent upon its own DNA, however, as nuclear genes in the cell also affect mitochondria function.  Fertile pollen can be restored by cell nuclear genes such as the Rf1 and Rf2 that make T cytoplasm corn fertile.  Similar fertility restoration for C and S cytoplasm sterility and be restored with presence of specific genes in the nuclei of the cells.
 
Plastids in cells function locations of starch storage and, in leaves, as the site of photosynthesis.  These chloroplasts also have their own DNA with about 104 genes.  Corn is among the few C4 plants the process photosynthesis in two distinct types of chloroplasts. Those in the main leaf cells do the initial process but final steps are carried out in chloroplasts in the bundle cells surrounding the cells. This is reviewed in Corn Journal blog of 7/14/2020 and 7/1/2020.
 
Corn hybrid genetics are mostly affected by the combination of specific nuclear genetic combinations of the two parent inbreds. Because only the female parent contributes the genetics of mitochondria and plastids choosing which parent is to be the female can have a drastic affect on some plant performance factors.  This can be dramatic with some parents having reduced germinations.  It is complicated and wonderful!

​Corn like other plants and animals have some DNA in cell organelles outside of the chromosomes in the cell nucleus.  Mitochondria are the site in the cell where carbohydrates are transformed into useable chemical form (ATP) for most energy use in the cell. It is an energy bound organelle in which these reactions occur. This Corn Journal blog in 2017 describes a dramatic interaction of corn mitochondria mutation and a devastating pathogen.
 
All living cells of plants and animals have mitochondria, organelles that convert carbohydrates into the useful form of energy that drives synthesis of metabolites in cells.  Mitochondria are believed to be descendants of bacteria that became symbiotic with cells in the early evolution of most living forms.  They retained their own DNA, are transferred to the next generation only in eggs cell and not sperm. They replicate within cells, but the host cells have some control on the rate of replication.  Energy conversion in mitochondria occurs on their folded membranes in a series of chemical reactions.  Regions of the plant undergoing rapid cell duplication have more mitochondria.  This includes the tassel cells of a corn plant.  The pollen mother cells in that region undergo meiosis and duplication, driven partly by the energy conversion by concentration of mitochondria in those mother cells.
 
A small defect in mitochondrial DNA of an inbred caused a defective membrane product in those mitochondria resulting in incomplete development of pollen.  This was found in a corn breeding program in Texas. As the inheritance of this condition was known to be only transmitted independent of nuclear DNA, it was called Texas male sterile cytoplasm.  It became a useful tool to corn hybrid seed production because it was easily transferred in breeding programs to the female parent of a hybrid, and thus avoiding manual removal of tassels in seed production fields. Use of T male-sterile cytoplasm became common in the worldwide corn in the 1960’s.
 
It was noted in the Philippines in 1961, that a fungal pathogen, then known as Helminthosporium maydis, was especially aggressive on several hybrids with T cytoplasm. Despite a few scattered reports elsewhere it was not until 1969 that the connection between increased occurrence of this disease and T cytoplasm became alarming.  Majority of seed produced for 1970 corn season had T cytoplasm, the main exceptions being new hybrids in which the conversion to sterility of the female parents was incomplete.
 
Although the pathogen was normally found in the southern half of the corn belt, and adequately controlled by products of nuclear DNA genes, this disease was found highly destructive in northern corn belt areas as well. A race of the fungus (now named Bipolaris maydis and by its sexual stage Cochliobolus heterostrophus) called race T, produces a toxin that causes death to cells with mitochondria having the DNA with the defect associated with T male sterility.  All cells of the corn plant with these defective mitochondria were vulnerable to the fungus.  This included the cells in developing seed resulting in diseased stored grain as well as overwintering leaves and stalks.  Normal resistance mechanisms to the pathogen were ineffective because the toxin destroyed these defective mitochondria.
 
As the relationship with T cytoplasm was realized, seed companies worked to change, and within a few years, the disease subsided back to its normal distribution.  It was a new learning experience of interaction of corn and pathogen biology.
 

​Fungi, bacteria and viruses have constant genetic mutations and evolution favor those that adapt to potential food sources.  This pathogen diversity must be matched with diversity in corn to avoid crop losses.  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. 
 
The fun never stops!
 
 

​Constant interactions with the corn plant biology, affected by its genetics, and pathogen biology, affected by its genetics, requires us to carefully observe potential changes.  Each participant in these interactions has potential for reducing our final product from the corn crop.
 
Bacterial pathogenesis of corn differs from fungal pathogenesis mostly because of biological differences in the two types of organisms.  Bacteria are single-celled organisms with a single chromosome without a nucleus in its cytoplasm.  Cell division in bacteria results in a new, distinct individual cell, whereas fungal cells divide to form a filament, frequently maintaining cell to cell communication and specialization.  Bacteria cell single chromosome simply replicates, then separates as a cell wall divides the cell into two halves, each with its own single chromosome.  Fungal chromosomes are enclosed in a nuclear membrane, divide by mitosis during cell division but also can undergo meiosis forming single strands of the chromosome and thus exist as haploids until the nuclei fuse to form diploids.  These structural and functional differences between bacteria and fungi results in different ‘strategies’ concerning adaptations of these organisms to changing environments.  Mutations occur in both, but those in the single bacterium chromosome immediately results in a changed new individual bacterium.  Mutation in fungal DNA may not take effect until recombination to form the homozygous recessive.  Bacterial biology allowing rapid reproduction of the new forms allows adjustment to new hosts.
 
Bacteria are ubiquitous, distributed by wind, water, insects and animals.  Rapid cell reproduction allows quick spread when in a nutritional environment.  Despite their widespread presence, most species cannot infect living corn leaves.  Leaves have evolved epidermal cells tightly held together and with a waxy covering, repelling water and prohibiting bacterial infection. Pathogenic fungi establish a multicellular mat (appresorium) from which it produces a penetration peg that enzymatically drills through the wax and epidermal walls to enter the leaf.  Bacteria cells can enter through open stomata-some even have flagella to help swim to the stomata. Plant resistance systems can produce antibacterial fumigants to inhibit the bacteria from replicating and there is some evidence stomata close when faced with bacteria invasion.
 
Small size and few visible structural features has made it difficult to identify a bacterium causing a plant disease.  Although some disease symptoms do become associated with specific species, confirmation usually requires culturing and chemical tests. 
 
It often takes a simple mutation in a potential pathogen, or in the corn host, for a relatively minor disease to become major.  Good for everyone in corn production to be aware as the crop grows.

​Virus genetics are probably the simplest of pathogens, some not even bothering with DNA but using mRNA to directly cause the host cell to provide the more complex process of DNA code as well as the ribosomes to produce essential proteins for the pathogen.  Fungal pathogens of corn have more complex genetic systems than viruses and corn.
 
​Corn reproduction is relatively easy to understand when compared to most corn pathogens.  Most corn cells have a single nucleus with 10 pairs of chromosomes with only the exceptions of the triploid cells of the endosperm and the haploid cells in the pollen and egg cells.  The hyphae of most corn leaf pathogens are filaments composed of multiple cells separated by cell walls called septa that have pores allowing exchange of cytoplasm and even nuclei. The nuclei are composed of a single set of chromosomes. Furthermore, a single cell of the fungus causing northern leaf blight may have up to 30 nuclei, all haploid.
 
Genetics of diploid cells are affected by both sets of the pair, generally with the dominant form of a gene on one set of the chromosomes resulting in the amino acid components of the protein and therefor the trait expressed.  Recessive genes get expressed only when both sets have the same recessive i.e., homozygous recessive for that gene.  Mutations resulting in new recessive genes are often ineffective because of the dominant form in the other member of the paired chromosome.
 
In a haploid nucleus, there is only one form of a gene, allowing a recessive gene to be fully expressed.  Resistance, especially those with single gene inheritance, in corn to a pathogen such as Exserohilum turcicum, cause of northern leaf blight, is initiated when the host cells recognize the presence a pathogens product (effector).  A mutation in the pathogen’s gene for this effector, negates the plants ability to recognize the pathogen and therefore this single gene for resistance is not initiated.  This is the weakness of the single gene system for resistance to any pathogen.
 
Fungal pathogens have the statistical advantage of producing new races because of the haploid nuclei in most hyphae.  For example, if a homozygous recessive form is crossed with a homozygous dominant, the first generation of a diploid organism would only produce the dominant gene product.  In the haploid hyphae, half of the resulting cells would produce the recessively inherited product.  This explains why some pathogens can successfully overcome the single gene type of resistance.  Being able to asexually reproduce with thousands of spores with haploid nuclei from the successful pathogen allows quick spread of a new genetic type.