Sugar is the product of photosynthesis, a process at which corn is especially good. The sucrose form of sugar is moved (translocated) from the photosynthetically-active leaf (source) to sinks such as growing leaves, roots and, eventually, seeds. Hormones, mostly cytokinins, direct direction of the flow.  Translocation occurs through the phloem portion of vascular bundles through cell membranes at the cost of some energy.  Cytokinins are mostly produced by the newly developing cells at growing points such as tips of root branches, leaf buds, growing leaf tips and embryos in newly formed kernels. We humans selected from the Teosinte ancestor, plants that not only met the minimal needs of producing seeds to assure a future generation to those with extra storage of carbohydrate in the fruit (grain) for our own consumption.  To do this we selected for excessive photosynthesis, temporary storage of excess carbohydrates in the pith of the stalk and eventual movement of it to the grain.  This was not done cheaply.  We had to get more leaf area and more root tissue to not only support the plants but also to uptake the water and nutrients to grow the bigger plant and to initiate the larger grains.  All of this required more energy.  After pollination, the newly formed embryo in each kernel begins to produce the cytokinins directing the flow of sugar towards it.   This is occurring at the same time that root tips are not as prolific and consequently producing less cytokinin. 
 
It takes about 10 days after pollination for the flow to each kernel to gain full speed. Varieties, and environments, differ in the flow rate per kernel but from day 11 to about day 40 the flow per kernel appears to be constant.  Production of sugars per day may be affected by cloudy days, or leaf damage but the power of the individual kernel sinks remains strong during that time.  Any shortage of new sugar is replaced by sugars stored in the stalk pith tissue. After the 50th day, the draw per day is reduced until finally an abscission layer is formed at the base of the kernel in which the phloem tissue no longer can move the sugars.  However during that 60-day period the root is competing with the kernels for sugars and our attempt to capture the maximum carbohydrate in the grain. Coming soon, the importance of sugars to the roots.

So, those 2-eared plants along edge of field die first, resulting in stalk rot.  How about back in the field, where bordered 2-ear plants are rare, is early death of the plant associated with kernel number?  An associate of mine, Eduardo Teyssandier, and I set out to compare prematurely dead plants with adjacent live plants in September 1976.  We randomly sampled variety display plots of many companies across 5 Midwest states.  All plants examined were bordered by others, and those with leaf damage or stalks broken from corn borer were noted but excluded from the study.  Forty hybrids were included, 112 pairs of plants studied.  The ones with rotted stalks averaged 561.9 kernels whereas the healthy adjacent plants averaged 459 kernels.  Repetition of the study in 1978 with 30 hybrids and 65 comparisons showed 647.5 kernels on dead stalks and 586.8 kernels on live ones. Differences were statistically significant at the 99.9% level.  Dead plants had 10-14% more kernels than live ones and yet the genetically identical plants were only a few inches from each other.  Also, in 1978, seven commercial hybrids were hand planted at density of 26100 plants per acre and at 34800 P/A to compare dead versus live adjacent plants.  In each case the dead plants had more kernels than adjacent live plants, although two hybrids had no dead plants when planted at the lower density.
 
It should be noted that these were commercial hybrids in the 70’s basically selected for performance at about 30% less density than is common in 2015.  They would be called flex ear types in today’s corn lingo.  Also it should be noted that all comparisons were made with adjacent plants within a variety and comparisons were not made between hybrids.
 
So, plants that show early death symptoms have more kernels than adjacent genetically identical plants. Also known is that pith cells of early death plants are depleted of sugar and senesce and that root rot precedes stalk rot.  What is the connection with these facts and the occurrence of stalk rot? How do breeders select for less stalk rot if genetically identical plants do not behave the same?

Pursuit to understand why and how corn stalk rot develops was certainly undertaken by many researchers before my attempts.  There were research publications done before corn hybrids were commercialized, when farmers mostly saved seed from the variety in the field.  But these plants were not genetically uniform.  Superior yields of hybrids and eventually the realization that highest yields came from single cross hybrids in the mid to late 1960’s, it became clear that even when each plant in the field was genetically identical, stalk rot could not be explained by genetics alone.  Pappelis at Southern Illinois University showed that the pith cells senesced after pollination and at rates faster in genotypes that tended to get more stalk rot.  Mortimore’s studies in Canada indicated that stalk rot is always preceded by root rot.  Ullstrup, at Purdue, did studies showing that root tissues start senescing soon after pollination.  Foley, at Iowa State, published that when the pith tissue pulls away from the stalk rind as when a plant wilts, the structural strength is reduced by 1/3 by simply changing from a rod to a tube.  Other studies showed that one could increase occurrence of stalk rot by artificially shading plants after pollination.  Corn borers were associated with stalk rot occurrence.  Leaf diseases like Northern Leaf Blight were seen to increase stalk rot.  Corn breeders were (and still are) frustrated that some of the highest yielding hybrids tend to be the most vulnerable to stalk rot.  Although pathologists usually identified a few fungi, such as Fusarium moniliforme, Gibberella zeae, Diplodia maydis, and Colletotrichum graminicola as frequently found in the dead stalks, actually many other fungi were also present.  But if root destruction occurred first, were these only quick invaders of tissue that was on its way to death?  And then there was the observation made by many that one often could see, in a corn row along the edge of a field, that the plant that wilted first had two ears, instead of the one ear on most of the other live ones in the same field.  Why that plant?
 

A dead plant with yellow lower stalk is adjacent to a genetically identical plant with a green live lower stalk. Why? I first hypothesized these could be the plants that emerged late, as if it developed from seed that germinated slowly because of deteriorating quality. In the field nursery with many hybrids tags were put by plants that showed only 3 leaves and other tags placed by seedlings just emerging when most adjacent plants were showing 5 leaves. These plants were followed through the season.  Late emerging plants definitely did not develop stalk rot. Some of those that were only emerging when tagged actually disappeared but if not they were completely barren. Those tagged with 3 leaves had narrow stalks and tassels that were much smaller and with fewer branches than surrounding plants, silks emerging later than other plants and averaged about 20% of the yield of majority plants- but no stalkrot.  I showed the plants to the fellow that evaluated winter growouts for purity of new seed lots. He said that confirmed his opinion that some plants he saw that looked like they could be inbred selfs were actually late emerging plants.  To make sure that these were not inbreds, the next year I hand planted 5 hybrids leaving interplant space for planting the same hybrids later between the initial planting.  These intentional late emergence plants looked the same as in the first year’s observation.  Late emergers apparently suffer from competition resulting in having very small stalks and yield but the stalks remain green.  Late emerging plants do not yield but also do not explain why adjacent plants do not behave the same in terms of stalk rot.
 
The concept that late emerging plants do not perform well and that seed quality is a significant component to good grain yields was observed by many others before that experiment in 1973, but it was new to me.  It also set me on path to find a better method of evaluating purity of hybrid seed lots as well as finding other explanations as to why a dead plant would occur adjacent to a green one only a few inches apart. It is probably significant that commercial hybrids of 2015 have a lot less ‘flex’ than those of 1973, but the basic importance of uniform emergence remains.

With a B.S. degree in Botany from Iowa State I was lucky to teach biology in Sarawak as a Peace Corps volunteer in 1963 and 1964.  Probably like all teachers, I soon discovered how little I knew about my subjects.  Among the many benefits of that job was the short term.  It was assumed that one would leave, and for me that meant grad school and a chance to learn more about plants and fungi. After more studies in Botany and Mycology I took a job with a seed corn company in which studies of plants and fungi was forced to face the realities of corn grown in many environments and considered as a crop instead of individual plants.  I was hired because of the corn industry concerns that their crop’s vulnerability to disease had been exposed with race T of southern corn leaf blight in 1970.  I, nor the seed company, had real clear ideas of what a plant pathologist should do in a company breeding corn seed varieties.  I had a lot to learn.
 
After southern corn leaf blight danger subsided, corn breeders advised me that their toughest problem was obtaining resistance to stalk rot.  So I was a guy with an interest in biology of plants faced with a complex problem.  Why does stalk rot occur in one plant but not the next?  Single cross hybrid plants are, at least theoretically, genetically identical. The fungi accused of causing stalk rot are ubiquitous and surely readily available to attach each plant. So, why this plant and not the next?

One of the more challenging concepts in agricultural science is how to study a very small aspect of the corn plant or a pathogen of corn and yet put it in the perspective of the affect on performance in a cornfield. Technologies that allow the studies of DNA code for a specific gene in corn are making remarkable additions to our understanding of a specific function in a corn plant.  Specific genes associated with different single genes for resistance to the northern leaf blight fungus can be identified by molecular analysis tests.  Of course, the fungus, without the ability to do molecular testing (LOL), nearly always has the genetic variability to take competitive advantage over others of its species to block the resistance component and cause the disease.  At least 5 single genes in corn have been identified that result in limitation in northern corn leaf blight, generally by not allowing the fungus to produce spores and spread within the field.  And, the fungus population is known to have at least 5 genes to overcome each of these genes.  Selection pressure for increasing the frequency of such genes in the pathogen population is pretty great when the resistance gene inhibits reproduction in individuals lacking these genes. 
 
We are witnessing this with insects and weeds as well. We can celebrate the attributes of genetic variability but also need to be aware that it sometimes works against our interests as well.
 
It is a problem for the grower of corn, the breeder selecting the next new hybrid, and the pathologist analyzing specifics of a particular disease to interpret data from small studies or observations into predicting how that will affect the performance in a specific 80-acre cornfield next year.  Probably all of us get excited to learn some new thing about corn but we can never forget that dynamics of growing corn in environments within a single field, let alone everywhere the crop is grown, is really, really complex. 
 
We all want to simplify but that is not reality of agriculture.  Just as in many other aspects of life, despite our desire for things to be simple, it is not.  Perhaps someone should mention this to politicians.

Those of us that attempt to maintain cultures of corn pathogens by growing them in artificial culture quickly become aware that isolates of the same species show considerable variability in growth rate, color, spore production and ability to infect the corn plant.  After several generations on the artificial culture media, some appear to lose the ability to infect plants.
 
Genetic variability in all living things comes from sexual recombination in which uniting of chromosomes from two individuals present new possibilities and form mutations.  A human geneticist once told me that humans have an average of 100 mutations, most of which are inconsequential but are different from their parents.
 
Fungi have sex, in which two ‘sexes’ combine and produce new genotypes that are some random combination of the two original parents.  The sexual stage for many corn pathogens is not easily found and therefore is assumed to not be common.  No problem for many fungi, however, because often their vegetative stage, the filaments (hyphae) of a fungus, often fuse, allowing their nuclei to join in a process similar to sex.  It is called parasexuality (outside of true sex) and can give the same benefit of producing new combinations of genetics.  The third source of variability comes from mutations. 
 
Variability is the source of survival and success of most species of plants, animals and fungi. Most pathogenic leaf fungi that produce enzymes to break down complex carbohydrates in plants basically have to kill the leaf tissue first to obtain nutrition for survival and reproduction.  The northern leaf blight fungus enzymatically drills into the leaf, grows towards the vascular tissue, plugs it up so it wilts at least in a area of a couple inches, killing that tissue. Now the fungus feeds on the dead tissue and produces more spores when moist, allowing it to spread and infect elsewhere on that and other corn plants.
 
If the plant’s initial resistance system cannot prevent infection of the veins, corn breeders have selected for resistance inherited by a single gene (Ht1) that inhibits the fungus from plugging the vein. Consequently the fungus is unable to survive and reproduce.  After being widely used for about 10 years, genetic variants in the fungus increased sufficiently to negate to use of that type of resistance.  The battle continues between genetic diversity in the fungus versus genetic diversity in the corn.

Corn is planted in all continents and certainly is productive in many temperate zone areas of the world.  But one important contributor to its success as a major supplier of carbohydrates to people and animals that they feed evolved in its original tropical past.  Most plants have a photosynthesis system with an inefficiency that limits its productivity.  This system, labeled as C3 photosynthesis, peaks in its ability to fully use total light intensity to about 3000 foot candles where-as unclouded sunlight has 10000 foot candles.  In corn, with it C4 photosynthesis, it continues to produce carbs in direct relation intensity of the light with maximum photosynthesis in bright sunlight.
 
Carbon dioxide enters plants through holes in leaves called stomata. These structures also allow oxygen to escape from leaves to the benefit of all of us.  Water vapors also go through the same stomata.  Stomata open and close.  At night they close with the benefit of avoiding unnecessary loss of water when photosynthesis cannot occur.  But when plant tissue is stressed from lack of water, these stomata also close, limiting the water loss but also interfering with uptake of carbon dioxide for photosynthesis.  C3 photosynthesis doesn’t make carbohydrates out of all the CO2 it absorbs, using some of it in other molecules.  No problem when environment provides plenty of moisture, is generally cool and have long summer days, but some plant species that evolved under hot dry conditions evolved systems to overcome that limitation.
 
Teosinte, the species of origin for corn in Central America, has a C4 photosynthesis system.  Plants with this character have additional structures in their leaves surrounding cells that perform photosynthesis. These cells function to reduce the loss of CO2 by causing these molecules to be recycled into more carbohydrates. The combination of extra enzymes and structures comes at some energy cost but the net gain is both more net carbohydrate and better utilization of CO2, even if stomata are closed. 
 
Fortunately, corn that was moved out of the original dry hot environment, kept that C4 photosynthesis system. Along with that came the C4 photosynthesis advantages and its superior production of carbohydrates.  Sorghum and sugar cane also are C4 plants but wheat, rice and soybeans are C3 and will not be able to match corn in carbohydrates per acre because of this trait. Although only about 3% of all plants species are C4, it does occur in a few plants in many plant families, suggesting that it can evolve independently. This would seem to raise hope that the efforts of the International Rice Research Institute and others trying to convert that C3 species to a C4. 

Corn’s history of genetic diversity has saved us from crop disaster from disease many times.  Although there have a few years of damage as a ‘new’ disease appears, the diversity available among corn breeding stock has always come to the rescue.  It is ironic that nearly all cases, the problem initially arises because of uniformity of the crop, for a few years combined with environments favorable to the disease.  Once recognized and main factors understood, seed suppliers select resistant genotypes, and that disease is reduced in significance.
 
Southern Corn Leaf Blight, caused by Bipolaris maydis race T, was the most significant in USA and elsewhere in 1969-70.  Genetic mutants of cellular mitochondria (the site of energy transformation in each cell) which allowed for cost-efficient seed production was not expected to be susceptible to a toxin produced by a strain of a fungus that was normally controlled by chromosomal genetics of corn.  Once recognized, however, the seed industry was able to switch to the resistant cytoplasm. It was very unusual that most of the industry was using the same source of genetic vulnerability, of course, but it was also relatively easy for everyone to switch within 2 years.
 
Most often the outbreaks have been much more limited to only a few genetic sources and the diversity already in corn breeding programs allows for adjustments once the source of susceptibility is understood.  With each the solution has come through good diagnosis by public and private plant pathologists, analysis of sources of susceptibility and recognition of sources of reasonable levels of resistance from current supplies of corn genetics. Not each experience has been exactly identical but in near future blogs I intend to review several of these ‘new’ diseases.
 
One of the good aspects of the southern corn leaf blight was it convinced corn seed companies that they should hire plant pathologists at the time I was looking for a job.  So, in 1972, I got lost in the corn field and have yet to find a way out.

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.