​​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.