Germination of a corn seed depends upon a rapid metabolic change in the cells from the minimal respiration occurring in dry seed to cell elongation in the root (radical) and shoot cells.   This requires mitochondria to activate after the seed imbibes water.  Rapid swelling of the mitochondria may cause breakage of the membranes but they do have the capacity to self repair.  Energy supplied by heat affects the rate of metabolism in seed and thus the rate of membrane repair.  Seed with significant membrane injury upon imbibition are slower to repair under cool soil temperatures than in warmer soils.  The delay in repair may be so severe that no germination occurs.
 
There is evidence that too rapid of swelling leads to more membrane breakage and consequently physical breakage of the pericarp allowing water to be imbibed faster and that is linked to germination reduction. Furthermore there is some evidence that seed treatments that reduce the rate of swelling can improve rate of germination in some seed lots. 
 
Each seed in a seed lot may be genetically alike but they had an individual history.  They differ in location in the seed field, time of pollination, health of the parent plant, moisture at harvest, placement in the drying bin, physical injury during shelling and handling, drying temperature and actual speed of drying.  They also vary in position of the ear that affects maturity and shape of kernel. The latter affects the position of the embryo in relation to the endosperm.  The trend of round seed with its protruding embryo to have lower germination rates than flat seed is believed to be due to increased vulnerability to physical damage during handling.  Given all of these variables it is amazing that we even get 90% germination in the field.
 

Mitochondria are not the only membrane source in corn seed cells.  Nearly all cell functions are carried out on membranes.  Endoplasmic reticulum (ER) is a major component of the cell which acts as transporter of the enzymes and proteins being produced in the cells.  It is also the transporter of the messages from the DNA in the nucleus of the cell.  Virtually all cell functions are dependent upon the structure of cell membranes.
 
Development of membranes in seed is dependent upon a combination of the genetics of the variety and the environmental stresses during seed development.  Drying the seed also significantly affects the membranes, as the membranes collapse with drying.  Corn seed producers are very aware of this potential problem and develop methods to assure that seed drying is carefully monitored so handling is gentle.  Seed membrane deterioration can occur in the field, especially if seed is allowed to dry slowly after fully developed at about 35% moisture when the abscission layer (black layer) cuts off nutrition from the plant.  Rain preventing harvest at this critical time is one cause of seed viability because it begins an aging process in corn seed.
 
A combination of drying temperatures below 100°F and quick drying by high air movement is critical to maintaining membrane integrity in corn seed.  Although all cellular membrane are probably affected by drying conditions, the fact that germination deterioration is mostly linked to the female parent of a hybrid, it is likely that the mitochondrial membranes are affected the greatest.  Each corn genotype varies somewhat in tolerance to these factors but the principles of drying temperatures and speed of drying appear to mostly involve membrane deterioration.  There is also some affect on the pericarp of the grain if it causes breakage.  Seed producers apply this knowledge and a lot of art to balance all the variables involved in producing seed with high field emergence rates the following spring.
 
 
 

As the early corn breeders moved a wild plant (Teosinte) into a grain crop with more carbohydrate storage in the seed, corn produced more starch than needed to produce the next generation.  Most of the grain’s carbohydrate is stored in the endosperm.  The embryo includes tissue adjacent to the endosperm called the scutellum that is rich in mitochondria and therefore ready to produce the energy needed to make enzymes such as amylases that break down the starch into it’s glucose components that will be moved to the other embryo cells.
 
Mitochondria show only slight activity in the dry seeds. Many apparently are only partially formed but a little respiration is occurring.  However, once exposed to water, and the seed imbibes, the cells and its components, including mitochondria, swell. Partially formed mitochondria are not only activated but gain the more membranes needed to get the glucose transformed into the chemical energy needed for germination. 
 
Studies have shown that temperatures affect this transition.  Not surprising to anyone experienced with growing corn, the mitochondrial activity is higher at 77°F than at 57°F.  Some of that activity is responsible for the membrane reproduction and repair not only in mitochondria but other membranes in the cells of scutellum and other embryo cells.
 
It is well established that the female parent of a corn hybrid is most closely related to ability to maintain high germination.  The fact that mitochondria have their own DNA and are transferred to the seed only from the female is likely a major cause for the relationship to germination.  Some studies have shown that differences in mitochondrial function under cooler temperatures are also related to the female parent as well.  Other seed characters are also female parent related.  A corn grain is a fruit with a thin pericarp, a female parent structure.  Endosperm cells are formed with two female shots of DNA and one from the male suggesting that also may have some uneven female parent influence.
 
The germination stability of commercial hybrids is dependent upon the choice of female parents, often to the chagrin of corn breeders.

Race T of Bipolaris maydis is not the only fungus that produced toxins affecting corn tCMS.  Phyllosticta maydis was not known to be an aggressive pathogen of corn until 1967 when first reported in Wisconsin.  It later became apparent that it was notable pathogen of tCMS only. The disease was called yellow leaf blight.  There was confusion about the species identification for a few years as another Phyllosticta species (P. zeae-maydis) was a common saprophyte on corn and was mainly differentiated by the size of conidia.  The toxin produced by P. maydis affected the mitochondrial membranes of tCMS about the same as the Bipolaris maydis, causing swelling and loss of the respiration function during energy transfer in the corn.  The switch away from the tCMS also essentially caused the  disappearance of this pathogen.
 
At least two other cytoplasmic sterile sources have become useful to the corn seed industry.  Both apparently involve some of the same mutation in mitochondrial DNA as tCMS.  These are designated as c cytoplasm (cCMS) and s cytoplasm (sCMS).  The DNA mutations apparently are slightly different in that they don’t appear to have the same vulnerability to the toxins produced by the fungi affecting tCMS.  There were reports from China that a race of Bipolaris maydis affected cCMS but I am unsure if that concern remains.
 
It is probably significant also that neither cCMS or sCMS are as effective as tCMS in controlling pollen production in all corn genotypes or even in all environments.  This makes them both slightly less desirable to seed corn producers as most do at least some detasseling in the seed fields when using female parents with either of these cytoplasms.

Plant and animal cell cytoplasm includes mitochondria and other organelles.  As discussed previously, the mitochondria function as the main source of providing chemical energy to the rest of the cell for growth, cell division and motility.  Mitochondria and chloroplasts also have their own DNA, provide their own division and multiplication and are only transmitted through egg cells in sexual reproduction.  The DNA in these organelles is relatively stable but occasionally have mutations that affect their function.  In many plant species this mutation affects the production of functional pollen.  In these cases, the inheritance being from mitochondria and only occurring in the cytoplasm, the sterility is called cytoplasmic male sterility or CMS.
 
This was discovered in a breeding plot in Texas in the 1950’s when an inbred was found to be male sterile.  It was related to a DNA mutation that affected one of the membrane layers of the mitochondria and the production of a polypeptide (URF13). The result is that the cell divisions needed for pollen production are inhibited.  There are nuclear genes, however, that result in production of proteins that overcome the negative affect of the mitochondria sterility affect and consequently result in production of pollen in a CMS plant.  These are called restorer genes (rf).  The Texas male sterile source (tCMS) was widely used in the 60’s because it allowed seed companies to reduce the expense of hiring people to physically remove tassels on the female parents in hybrid seed production.  The restorer genes were bred into the male parents or the non-sterile versions were mixed with sterile versions in seed sold to farmers so there was adequate pollen for grain production. 
 
In 1969 it was noticed that relatively minor disease in the southeast Corn Belt was suddenly more aggressive. Furthermore, it was much more damaging on plants with tCMS than those without this cytoplasm.  A variant of the fungus Helminthosporium maydis (now Bipolaris maydis) produced a toxin that caused mitochondria with the mutation to swell and destruct. This allowed the fungus to cause large lesions, produce more spores and cause more damage.  Because most of the seed produced in 1969 in the USA had the tCMS mitochondria, most hybrids planted in 1970 was susceptible to this race T of this fungus.  Although seed companies scrambled to build up non-tCMS seed supplies that year and because the August 1970 weather in much of the Midwest had warm humid weather favoring the fungus, grain yield losses approached 40%. 
 
Using southern hemisphere locations, seed companies increased non tCMS parent seed but still managed to only supply blends of tCMS and non CMS seed to farmers in 1971.  Fortunately the August weather in the Midwest that year was more of the drier and cooler night temperatures and the disease damage was limited.  By 1972, the disease was reduced to much more normal levels.

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.
 

Humans attempt to define each others race by a few recognizable physical characters that in reality represent, at most, 0.0001 of the total DNA of any person and that varies greatly among people from any one geographical or ethnic origin. And those physical features have nothing to do with any individual’s behavior.
 
Plant pathologists have even a greater problem in trying to characterize the genetic variation with a corn pathogen species. Not only do fungi offer few morphological characters to use for defining individuals, and those characters are mostly only observable with a microscope, the numbers of individuals are huge.  It becomes very difficult to take samples in order to estimate the range of characteristics within a species. Usually the term race of a pathogen is defined as it’s ability to overcome a specific gene for resistance in the host. 
 
Helminthosporium turcicum (sorry, I can’t shake the habit) was successfully controlled by a single gene in corn that was called the Ht gene. That single corn gene, first discovered in a popcorn variety, inhibited the fungus from plugging the vascular tissue in a leaf and kept the fungus from producing spores to spread elsewhere in the field.  It was widely used in the 1970’s by most corn breeders as it appeared to be effective everywhere in controlling northern corn leaf blight. Then, in 1979, it was discovered that a seed field in Indiana with the Ht gene was heavily damaged by the disease.  I had the same experience as other corn pathologists at that time to discover that the newly discovered variant of the fungus could be found in many midwestern fields.  So now the original population of the fungus controlled by the Ht gene was called race 0 and the new one as race 1.  Race 1 had a gene mutation that allowed it to overcome the resistant gene in the host.  Since then at least 4 more single gene resistance sources for resistance to this pathogen have been found and likewise every combination of fungal genes to overcome these genes have been found in the fungal population have been identified.  These are all given distinct racial identities. But just as with the limitation of human racial descriptions, these designations depict only a small, limited description of the variability among individuals of the population.  With the outbreaks of northern leaf blight in much of the USA Midwestern corn belt in 2015, I was asked if it was a new race.  Probably not, but most likely a population of the fungus favored by many environmental factors and many genes. 

Three centuries ago, Linneaus came up with a system of giving names of all living organisms.  It included a genus name to include closely related plants and animals and a species name for individuals that were distinct and supposedly would remain distinct by not interbreeding with other species.  It is a universally accepted method to allow communication across languages attempting to assure that all are addressing the same organism.  Identification of plants generally emphasized the sexual reproduction stage as a distinction, as morphology of the flower often affects genetic isolation of a species. The ‘scientific’ name of an organism is usually in Latin and consequently is italicized when included in English text.
 
But what to do with those organisms that are known only to reproduce asexually but later discovered to have a sexual stage as well?  The name for the genus Helminthosporium was created to include fungal species with elongated, multi-cellular, dark pigmented, asexually-produced spores (conidia).  The name was created because of the similarity to a group of parasitic worms called Helminths.  Helminthosporium species are largely pathogens of grass species such as corn, oats, rice, wheat and turf grasses. Helminthosporium maydis, causal agent of southern corn leaf blight, H. carbonum causes northern leaf spot and H. turcicum causes northern leaf blight. Each of these species primarily spread via the conidia and the shape of the conidia as it appears under a microscope is diagnostic for the species.  Then the sexual stages were discovered as well as a few other conidial distinctions.  H. maydis and H. carbonum not only share a similar sexual reproduction structure but also the conidia germinate in a similar manner from each end of the spore. Thus the asexual genus name for these and some others was changed to Bipolaris and the name for the sexual name is now Cochliobolus.  So the cause of southern corn leaf blight is now Cochliobolus  heterostrophus or Bipolaris maydis. Northern leaf spot is caused by Cochliobolus carbonum or Bipolaris carbonum.  As if this is not confusing enough, it is also known that these two species can cross, causing all sorts of confusion in names, as will be discussed in a future blog.

​Helminthosporium turcicum conidia have distinctions from some others of the original genus so now are grouped together with similar morphology as the genus Exserohilum. The sexual stage also has been identified making that name as Setosphaeria turcica.  To communicate on a practical basis, most corn pathologists refer to the cause of northern leaf blight as simply Exserohilum turcicum and some of us old guys have trouble avoiding the use of Helminthosporium turcicum.  Most non-pathologists prefer to simply name the disease and forget all about naming the fungus, and that is ok too.