​Corn genetics and planting rates have changed a lot in the last 50 years.  Breeding and selection of hybrids when planted in the USA Midwest at 22000 plants per acre required different genetics than when planted at 36000 plants per acre.  Plants had more kernels supplied by more photosynthesis per plant. Higher densities with those hybrids would certainly develop the photosynthetic stress dynamics resulting in stalk rot because of insufficient carbs to supply both the grain and roots.  More plants per acre, and slightly smaller ears per plant allowed a total of more grain, compensating for the reduction in photosynthesis per plant.  On the other hand, these types of hybrids are more reliant on getting maximum number of productive plants.  This is not only the necessity of high number of germinating seed but also that the seedling emerge uniformly.  This was discussed in Corn Journal on 3/10/2016.
 
40 years ago, when pursuing the question of why one plant died early with stalk rot and the adjacent plant did not, I hypothesized that the dead plant was that one emerged late as a seedling.  When most of the plants in the test plots showed their 5th leaf, a tag was put near those that had only 3 leaves and another marking those with only a spike.  Notes were taken of these plants and their adjacent plant during the season.  At pollination, it was clear that even those tagged at three leaves were not silking in time with adjacent plants and tended to have more slender stalks. Many of those tagged as spiking no longer were present, but those that survived were far off in pollination timing, had very small, narrow stalks and, eventually, small tassels.  Ears were harvested at end of season and kernel numbers were counted. Those tagged with three leaves had only 20% of kernels of adjacent plants and those tagged as spike only were barren.  Delayed emerging plants did not develop stalk rot but clearly the delay affected yield.
 
To eliminate the possibility that these delayed plants were not ‘selfed’ inbreds instead of hybrid plants, an experiment was performed the next season to confirm that emergence delay was the main factor.  Seed was planted with twice the normal plant-to-plant spacing. When those seedlings spiked, the same hybrid seed was planted between the seedlings.   This would be an unusual delay, but the effect was the same as the first observation.  Barren plants, skinny stalks, small tassels were characteristic of the delayed emergence. Apparently, plant competition for late emerging plants has a drastic affect. 
 
Others have done similar experiments before and after these done by a young guy beginning to learn about corn.  My conclusion was that individual plants developing stalk rot were not the late emerging ones and that uniform emergence was an important factor in corn yields.  Also, it was interesting that those late emergers could be confused with selfs, as confirmed by the fellow who normally evaluated hybrid purity in winter growouts.  That eventually led to developing a different purity test method.
 
My experiments were done in the 70’s with hybrids and plant densities common at that time.  It would be useful if similar experiments were done with more recent hybrids selected for consistent ear development at the higher plant densities used today.  It is notable that experiments done by others have shown that among germination test methods, the cold test is the best predictor of field emergence and that it accounts for about 70% of differences among seed lots in field emergence. 

​Corn seed germination quality is always temporary.  Female seed parent genetics, especially that of the mitochondria, area factor.  Seed with dormancy because of low moisture content remains alive as long as the mitochondria have a low level of respiration to maintain membrane integrity, it becomes more difficult if kept in humid environments at temperatures greater than 50°F.  We have seen many examples of seed kept on farms because 2019 weather prevented planting.  Some will show in the field this spring.
 
Perhaps, for the first 8 centuries of corn culture, the percent of seedlings emerging from seed planted was not as significant as the amount and type of grain produced.  Planting in hills or even by planters at low densities, favored genetics that produced larger ears if adjacent seed did not germinate.  Modern terminology attempts to identify hybrids that adjust of lower density by producing larger ears defining them as ‘flex’ ear types.  It is doubtful that there are only two types, flex and non-flex, but hybrids do have different tendencies when plants are less dense.  There are hybrids that will tend to go barren if planted too dense and there are others that will only show competitive yields if planted at high densities.  There are some that do not cut back on kernel numbers if crowded but will develop high percentage of stalk rot if planted too thick.  Recent years of corn culture in the USA has led to hybrids that tolerate planting a 33% higher density than 40 years ago- and give more stable high yields than hybrids of that era.
 
These modern hybrids may have genetics for more photosynthesis per acre, at least due to increased leaf area, but also consistent silking when under the stress from competing plants.  This may also favor selection of hybrids with less ‘flex’ and consequently a need for higher plant density.  Although best knowledge of the ideal plant density in any season only becomes apparent after harvest, there is more pressure now than 40 years ago to have a uniform emergence percentage of 90+% every season.
 
Every seed within a single cross hybrid may be nearly genetically identical, but not with identical germination quality and not planted in identical microenvironments.  Highest quality seed will tend to emerge uniformly, and seed producers make large efforts to produce such seed.  However, even with best genetics, timely seed harvest and care in handling the seed it is rare that field emergence is perfect.  It is a challenge to produce all seed lots with great quality and for testing systems to correctly predict the field emergence the following spring. 
 

Corn seed dried properly to less than 15% moisture allows the mitochondria in the embryo cells to remain intact. Respiration in these mitochondria continues at a very slow rate, releasing sufficient energy to maintain membrane integrity of cell organelles.  Genetics, especially of the female parent that supplied the mitochondria from its egg, affected this success as well as the physical conditions during seed development and harvest. Success gets revealed when the seed is planted. That process was described in Corn Journal blog 4/25/2017.
 
Very soon after the corn seed is planted, imbibition begins. The H2O activates the membrane-bound mitochondria to respire, providing energy for protein production. The enzymatic proteins include those that digest the starch stored in the endosperm into more sugar molecules to be transported through the scutellum to other cells in the embryo, resulting in more energy available to produce structures for cell elongation.  Heat energy provides a regulatory function affecting the speed of this germination process.  Imbibition occurs at any temperature but metabolic activity in corn is generally thought to be very low if seed environment is below 50°F.  Speed of germination increases as the temperature increases.
 
Membrane integrity within the seed also affects the net speed of this process.  Those individual seed with more damage are slower to sufficiently activate the system and thus slower to activate the metabolism needed for cell elongation in root (radicle) and the shoot sections of the embryo.  Cool environments, delaying membrane repair, may result in death of the imbibed seed before the shoot can emerge from the soil.  Some of these seed, even after warmed manage only to extend the root through the outer wall for the kernel, the shoot never emerging.  Other weakened seed may finally get enough momentum to push through the soil surface but days after the healthier seed have emerged, resulting in a season-long competitive disadvantage.  Heat energy during germination affects the severity of the effect of membrane damaged seed.
 
Microbes in the soil are generally warded off by products of seed metabolism in healthy seed. Those individual seeds that are slow to generate sufficient energy for growth are also more easily attacked by microbes, further slowing the germination process.  Seed treatments are useful in giving the damaged seed more time to successfully germinate. Healthy seeds can successfully produce normal seedlings despite surrounding common soil microbes but those weaker individuals need the extra protection.

Imbibition is the movement of water through a membrane. This occurs in a corn seed when placed in a moist environment.

Corn seed, dead or alive, will allow water to enter through the pericarp, causing the kernel to swell. Dry cells in the embryo retain many membrane-bound structures including mitochondria, plastids including chloroplasts, nucleus and endoplasmic reticulum.  Cellular membranes are composed of phospholipids and proteins organized in a manner that regulates the biological function of the cell organelles including regulation of movement of products in and out of the organelle. 
 
Membranes in a dry corn seed cell are only slightly active, oxygen to pass through, for example but have more of a gel like structure.  Within a few hours of imbibition, the structure changes as the phospholipids become moist and swollen.  Resulting metabolism with activation of respiration in mitochondria, fueling gene translation in the nucleus, movement of RNA on the endoplasmic reticulum and production of protein in the ribosomes.  The water plus metabolism causes the radical part of the embryo to elongate and the germination process has begun.
 
Two potential problems can stop this process.  The seed may no longer have sufficient structural integrity, possibly because the aging process while dry no longer maintained the metabolism needed for maintenance.  A second problem can be that the imbibitional process caused breaks in the membranes that were not adequately repaired during those first few hours of swelling as water moved into the cells.  Membranes do have the capacity to self-repair and often do when metabolism is active.  However, this process is temperature related, and in corn this repair process is very slow when temperatures are at about 50°F.  Imbibitional chilling injury is the term used to reflect poor germination of some seed when planted in cold soils. 
 
Every seed within a lot, although genetically identical, has had a slightly different environment experience.  Location on the ear, exposure to insect or fungus, location in the drier, handling in the sheller or bagging processor all could affect its tendency to cellular injury.  This usually if most profoundly expressed when it imbibes water under cold conditions.  Some seed may reflect this by only delaying the germination as it repairs sufficient membrane for metabolism to germinate although later than the other seeds. 

​From Corn Journal 03/08/2018

After overcoming the leaf surface protection against fungal invasion, the battle inside the leaf begins. This corn journal blog in 2018 illustrates the next phase of the battle between host and pathogen. 

​A recent report in Science (Vol.359, 1399-1403) describes how a single fungal gene controls plant cell-to-cell invasion by the rice blast fungus.  It is an interesting description of how a plant pathogen manages to invade a plant cell and manages to travel cell-to-cell, evading the plant immunity system, eventually killing significant sufficient tissue to sporulate and spread to other plant tissue.  This study involved a lot of biochemistry and microscopy and uncovered interactions that are probably common to other fungal-corn interactions.
 
Living plant cell walls have microscopic holes, called plasmodesmata, that allow passage of sugars and proteins to adjacent cells.  These holes are smaller than normal fungal filaments (hyphae).  In this study in which the pathogen Magnaporthe orzae, cause of rice blast disease, initially invades the plant by forcing the outer leaf cells with an appresorium, to occupy a cell but maintaining the cytoplasm in the cell.  The hyphae of this fungus reduce the size of the hyphae to about 1/10th to squeeze through the plasmadesmata into the next cell.  The plant cell resistance includes reacting to the presence of the invader by depositing callose to close the plasmodesmata, and therefore restricting the fungus to the initially invaded cell.  The researchers found that a single fungal gene delays the resistance reaction until the pathogen has passed on the next cell.  Mutants of this gene in the fungus are not able to pass onto the next cell. Resistance is related to a quicker reaction in closing the plasmodesmata as well as repression of the fungus within the infected cells.
 
This study involving the interaction between a fungal pathogen and host is probably common to many leaf diseases.  Relatives of this fungal species attack other grass crops such as wheat and barley but apparently not corn. The study illustrates the evolution of methods of attack by pathogens and competing defense systems by plants.  It is also interesting that the study was done by several specialists employing multiple techniques and understandings of their science. 

​The continual battle between the carbon producer, like corn, and the organism seeking carbon nutrition involves biology of both organisms.  Each corn pathogen has evolved different biological features for success.  Exserohilum turcicum, the fungus causing northern leaf blight of corn produces spores (conidia) with thick wall that do not immediately desiccate, germinate within a few hours of exposure to moisture and set up an appresorium and penetrate the leaf surface within a single day.  The relatively heavy spores tend to not travel far within a field from the original infection site.
 
Cercospora zeae-maydis, cause of gray leaf spot, by contrast has relatively thin-walled conidia that germinates on leaves with only high humidity (80-90% RH). After germination the mycelium remains on the leaf surface until being exposed to 95% humidity for a total of nearly 100 hours.  The mycelium can tolerate as low as 60% humidity in a somewhat dormant and then continue to grow when higher humidity returns. After meeting the minimum, an appresorium forms and the fungus enters to leaf surface. The thinner walled spores of Cercospora zeae-maydis is more easily moved in the winds and therefore spreads easier within a field.
 
Common rust fungus, Puccinia sorghi, is even more easily spread in the wind.  Spores (urediniospores) have thick walls but are round and about a third the size of the E. turcicum spores.  Thick walls prevent desiccation allowing long distance travel and light weight encourages it.  The spores cannot withstand the absence of susceptible hosts between live corn presence during the temperate winters.  Consequently, production of a new urediniospores occurs in more tropical areas with continuous corn growth.  High altitude winds carry the spores to the temperate zones where new corn plants are growing.  These spores quickly germinate in moist corn leaf surface, germinate, then an appresorium above a stomata, penetrating the leaf. This requires about 6 hours of moisture.  The leaf whorl, always moist, fits this process.  New spores are quickly produced and spread within the field can happen quickly.
 
These are three examples of corn fungal leaf pathogens with different infection and biology.
 

The disease is caused by the fungus Exserohilum turcicum (Setosphaeria turcica).  The fungus lives in infected, dead or live leaves.  It asexually produces spores (conidia) when the diseased tissue is moist and temperatures are proper for corn growth.  The conidia have 4-6 cells arranged in a row and are light enough to be distributed by air currents within a corn field.  After landing on a corn leaf, with a little moisture, in 3-6 hours the cells on both end of the conidia, begin dividing, emerging as germination tubes. These new hyphae quickly form a base on the surface called an appresorium, from which the fungus grows into the leaf epidermis.  Within 12-18 hours after the conidia have landed on the leaf, it has successfully penetrated the leaf.  There appears to be no difference in time to leaf penetration between the susceptible and resistant corn hybrids.
 
Chloroplasts near the infection point soon lose pigments as nearly 100 cells die, perhaps because of enzymatic activity of the fungus.  This can be observed when small (0.5-1cm) circular, yellow spots show in the leaves in 24-48 hours after infection.  From this initial location, the hyphae grow between cells towards the vascular bundles.  Penetration of the vascular bundles is followed by plugging the xylem causing further death of surrounding cells dependent upon the water supplied through these tubes.
 
Resistance systems appear to begin after initial infection and perhaps mostly once the fungus has reached the vascular system.  There does seem to be differences in that initial yellow spot in a couple days after infection and I wonder if the brighter color is not associated with greater quantitative resistance.  Could be part of quantitative resistance or be self-destruction of cells near the infection point, depriving the fungus of nutrition?  It does seem that initial spot is less obvious and possibly smaller in the more susceptible corn genotypes.
 
The wilted areas surrounding the plugged xylems eventually are depleted of living host cells. The fungus responds by producing new conidia within 14 days of the initial infection, ready to spread to more live leaves.  Exserohilum turcicum remains viable in dry leaves for a number of years in dry environment, ready to produce conidia within 24 hours after moistened.  Tillage, crop rotation and hybrid resistance become major factors in crop damage from this disease.
 
Much is written about this disease.  An interesting summary of the morphology aspects is included in this report: Journal of Applied Biosciences (2008), Vol. 10(2): 532 - 537.  ISSN 1997 – 5902: www.biosciences.elewa.org (From CornJournal 11/21/2017).

​Corn leaves are constantly surrounded by fungal spores during the whole season.  The waxy leaf cuticle and tight compaction of the epidermal cell walls inhibit penetration by the vast majority of fungi.  Even entrance into the leaf through open stomates is restricted by antimicrobial fumes from the cells inside the stomata.
 
A relative few fungi have methods to overcome these defense systems. Spores of Exserohilum turcicum, the pathogen causing northern leaf blight, germinated within a few hours of exposure to moisture on the leaf. The hyphae growing from the spore responds to the surface hardness producing mucilage promoting adhesion to the leaf surface.  Soon the tip of the hypha forms a special cell called an appresorium.  Exposed cell wall of the appresorium cell thickens but the wall adjacent to the leaf surface remains thin.  The cell gains turgor pressure from moisture as cytoplasm in appresorium cell absorbs glycerol from the fungal spore hyphae. Turgor pressure results in formation of new cell that forces through the leaf cuticle and through the epidermal cell walls. 
 
Penetration into the corn leaf by the pathogen causing northern corn leaf blight occurs about 10-12 hours after the spore and moisture on the leaf surface. Favorable environment for spore germination and appresorium development usually is present in the whorl of pre-flowering plants, with fog, high humidity and dew formation. 
 
The battle between plant defense systems and pathogen offense continues.
 

​Resistance to leaf diseases in corn that limits the number and size of lesions is called horizontal or quantitative resistance and usually involves 3-5 genes.  Ratings for this type of resistance involve a scale developed after considering disease pressure from different environments but does provide a stable type of resistance. Resistance to some leaf pathogens can have another system, usually involving a single gene, that stops some races of a pathogen more completely than horizontal resistance.  This latter type of resistance is called vertical or qualitative resistance.
 
The Ht1 gene was discovered in 1964.  It prevented the northern leaf blight pathogen, Exserohilum turcicum, from developing the normal wilted lesion symptom after it reached the vascular tissue.  Instead of the normal lesion formation, a small yellow streak developed and, most importantly, the fungus failed to reproduce with spores capable of spreading the disease within the corn field.  This seemed ideal in the USA because its presence was easily identified and damage from the disease was eliminated.  Consequently, the Ht1 gene was utilized in commercial hybrids during the 1970’s.  In 1979, a race of this fungus was found in several locations in the U.S. Corn Belt that overcame the Ht1 gene resistance, resulting in normal lesion and sporulation.  It appears that the fungal gene responsible to overcome the Ht1 gene was present in a low frequency within the widespread population of E. turcicum.  Its frequency increased as it gained competitive advantage over those individuals without this gene.  Similar races of this fungus had already been noted in South Africa and the Philippines.
 
Other single genes (Ht2, Ht3, Htn) for resistance to E. turcicum have also been identified, as well as races of the fungus that overcome those resistance systems.  This is not a new phenomenon.  Genetic diversity within pathogens have repeatedly shown an increase of individual genes producing products to overcome single gene resistance.  It should be noted that the term race for a pathogen refers to only a single gene difference within the pathogen population.  It probably existed as a mutation, allowing a slight structural change in a protein that happened to be attacked by the host plant’s resistance product.  Qualitative, vertical resistance to a disease in corn offers quick answers but stable, long-term benefits are best when quantitative, horizontal involving several genes are employed in corn hybrids.

​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.  (Corn Journal 7/11/2017)
 

​Corn cell structures and functions are affected by environment. Water supply to the cells influences plant function throughout its life.  Imbibition of the seed initiating the cell elongation of cells and their functions occurs only when water concentration surrounding the seed is sufficient. Cell elongation driven by turgor pressure pushes the roots down and shoot up through the soil. 
 
At about the V5 (5 visible leaf collars) the growing point differentiates into a tassel.  It is all cell growth now. Cell elongation in the stem cells as well as in the leaf cells is greatly affected by water pressure within the cells.  Warm wet conditions consequently result in taller plants and larger leaves.  Kernel row number is set by V6 but the number of kernel ovules per ear is affected by the water pressure.  Dry conditions resulting in few kernels and smaller tassels.  Drought also can reduce the opening of the stomata and consequently less CO2 intake and reduced photosynthesis.  Energy for the cell growth is provided by photosynthesis, the sugars guided to the various sinks in roots, leaf tips, shoots and tassel. The uppermost leaves get the direct sunlight allowing the highest photosynthetic rate.  As the canopy closes in, the lowest leaves receive only a fraction of the light, sometimes not producing enough carbohydrate to meet respiratory needs for normal metabolism.  These lowest leaves often become susceptible to relatively weak pathogens, develop yellow spots and drop off. By V6 stage the corn plant growing point is not putting out new cells, differentiation is over and now it is up to the dynamics of cell elongation to determine final plant development.
 
Genetics influence the root growth direction.  Hybrids with a tendency to be highly branched near the soil surface are adapted to absorb and transport more water from organic material near the soil surface but may have trouble reaching deep into soil during drought conditions.  Hybrids that tend to have fewer branches near the surface, but extremely deep roots may excel in drier conditions but can be more vulnerable to lodging in strong wind conditions.
 
Larger leaves, expanding due to leaf cell water supply, may have potential for more photosynthesis per plant. Larger leaves also have potential for more stomata increasing the supply of CO2 but also the loss of water via transpiration.
 
The corn plant’s interaction with water occurs at the cellular level.  The cell’s response is affected by genetics and other environmental influences such as minerals, light intensity and pathogens. It is complicated!
 
 

Among the specialized cells in corn leaves are the stomata.  Each stomate consists of two guard cells and two companion cells. Corn, being a monocot, has these specialized cells organized parallel to the length of the leaf at a rate of about 36000 stomata per square inch on the top of the leaf and about 50000 per square inch on the bottom to the leaf. 
 
Blue light wavelengths detected by a carotenoid activates a process in which potassium ions flow into the guard cells.  Thus, the water concentration in the cell drops, resulting in osmotic pressure for water to enter the guard cells.  The shape of the guard cells allows uneven swelling and a pore opening up between the two guard cells.  Photosynthesis produces sucrose that then contributes to the osmotic pressure in the cells.  At the end of the daylight, starch is synthesized from the sucrose and potassium ion concentration is reduced and the opening between the two guard cells closes. Other compounds within these cells also contribute to this phenomenon. https://academic.oup.com/jxb/article/57/2/381/489968.
 
This is essential, of course, to allow diffusion of CO2 into leaves for photosynthesis in other leaf cells. Open stomates allows O2 to be released to the atmosphere but also water loss. Water evaporation through stomates (transpiration) is affected by the relative humidity in surrounding atmosphere as the water concentration within the leaf spaces is nearly 100%. Cohesiveness of water molecules ‘pulls’ water up to the leaves so that essentially every molecule of water that goes out the stomata is replaced by one from the root tissue.
 
During the day, stomata are open, carbon dioxide moves into the leaf, oxygen moves out and so does water.  At night, photosynthesis in the guard cells stops, water moves out of the guard cells causing the swelling to be reduced and the pore is closed.  We will discuss more about this phenomenon later as the plants grow.
 
Stomata are essential to corn and have a dramatic affect on productivity as import of carbon dioxide and export of water occurs through the stomata.  This topic is covered in Corn Journal 5/10/16.
 

​When the plant apical meristem cells interpret the combination of daylight length and accumulated heat, as determined by genetics, the terminal shoot meristem and at least one of the meristems located at a stem nodes, begins to produce cells for the tassel and shoot.  Resulting modified stems and leaves now produce the male and female flowers of the corn plant.
 
​Maize male and female flowers are on separate branches of the corn plant, thus the species is called monoecious, as opposed to the dioecious flowers of soybeans.  Both the ear-forming branch and the terminal tassel is composed of multiple flowers.  Each kernel that forms in the ear traces to a single flower with a single ovule within the fruit wall, the ovary.  Both male and female flowers of corn begin as dioecious but the male portion in the ear and the female flower in the tassel are aborted very early in the development of each.  A mutation or an environmental factor can overcome the abortion, resulting in tassel seed or terminal tassel on an ear.
 
A corn tassel may include up to 1000 spikelets, each one including 2 florets.  These individual flowers are enclosed in the modified leaves called glumes.  Each of the florets have three stamens, consisting of filaments and anthers.  Each anther includes multiple cells called microspore mother cells or microsporangia.  Meiosis occurs in these diploid cells resulting in 4 haploid microspores per mother cell.  This occurs over a period of 3 days.  Microspores become free of each other as they grow for a few more days.  The individual haploid nucleus in each microspore undergoes mitosis, resulting in two haploid cells within the individual pollen grain.  The pollen grain secretes a pollen wall within another 7 days.  Starch crystals accumulate within the pollen grain during that wall formation period as the cytoplasm of the pollen grain dehydrates.   A small pore is formed in the pollen wall. 
 
Pressure from the growing pollen grains and dehydration of anther walls causes the split that allows the release of pollen grains.  One thousand spikelets each with 2 florets with three anthers each with hundreds of pollen grains easily produces a cloud pollen.  Production of the spikelets over a period of days results in daily release.  Pollen longevity may only be a few hours in high heat but the release over consecutive days in a field of corn usually assures viable pollen reaching most viable female stigma.
 
The remarkable human selection and development of maize adapted to multiple environments because of available genetic diversity is largely due to the separation of male and female flowers.  (Corn Journal 7/17/18)
 
 

​New above-ground cells are produced with cell division in the apical meristem. Genetics and environment control the eventual size and function of those new cells.  This was addressed in the Corn Journal Blog on 8/8/2019:
 
Corn shoot apical meristem is genetically controlled to switch from producing new leaf and cells to the terminal male flowers of the tassel.  The main environmental factor influencing this switch in temperate zone corn is heat energy.  Earlier maturing corn requires less heat to trigger this change in apical meristem products, allowing corn to mature in short seasons far from the tropical environments of corn’s origin. 
 
Plant height is determined by the number of cells produced by cell division at the apical meristem before switching to producing the cells that becomes the tassel and the elongation of the cells.  Elongation of the stem cells is enhanced by water pressure applied to the young cells before maturing with less flexible cell walls.  Thus, water availability to the roots, root volume and transport of water to the expanding cells in upper plant also affects the eventual plant height.
 
Corn planted later than normal in temperate zones, accumulating heat units quicker than usual, produce fewer stalk cells because apical meristem is induced to produce tassel cells quicker.  If water availability for cell expansion is less than optimum, the result of these two factors will be shorter plants than usual for a hybrid.
 
 

​Corn stalk cells of the rind have thick walls with lignin, hemicellulose and cellulose, all carbon-based compounds formed after carbohydrates were shipped to the stem locations.  Rind cells are major barriers to pathogens and insects and contribute to the withstanding of lodging pressures.  Hybrids vary in the thickness of the rind with strength measured with special penetration equipment.  
 
Stalk pith tissue is composed of parenchyma cells with thinner walls allowing import of sugar molecules. Cytoplasmic activity in these cell plasmids converts the glucose into starch molecules.  This functions as an energy storage for future use in roots and grain, as hormones directs the movement.  As grain begins to form, sugars are moved at a steady daily pace.  When stresses, such as leaf disease, or hail damage to leaves or cloudy weather reduce photosynthesis, the reserve from the stalk cells is pulled to the grain.  
 
Vascular tissue in the stalk becomes the vehicle for the movement to the grain and root, while the xylem supplies moisture to the stalk cells from the root.
 
Stalk pith cells connect to the rind cells, essentially a solid rod of the stalk and thereby adding to the stalk total strength.  Some have estimated that this is about 33% of the total stalk strength.
Movement of sugars to the grain can result in deprivation of sugar needs for root tissue, resulting in early death of root tissue.  This reduces the uptake of water by roots eventually causing the leaves to wilt and the stalk parenchyma cells to collapse.  The latter results in pith cells to pull away from the rind, essentially changing the rod structure to a tube. Death of these cells allows the advance of fungi as active cell metabolic resistance is no longer effective.  Consequently, the stalk easily lodges.  We often refer to these as stalk rot as fungi present are identified.  The real problem, however, was the starving of roots.  
 
Photosynthetic stresses combined with the draw of sugars to the grain reduced the available of chemical energy for root cells. Death of the root resulted in wilting of plant and redaction of stalk pith cells. Withdrawal of the pith cells away from the rind cells weakened the strength of the stalk.

​Cells of the corn plant are the source of the plant structure and function.  Converting light energy into chemical energy allows for growth and production of cell structures and chemical compounds allowing for all of living cell function.  The totality of construction and function of the plant is determined by its DNA and interaction with environment.  Ultimately, however, the movement within the plant of different cell products requires communications among the cells.
 
Movement of water within the plant is mostly made by simple physical principle of diffusion and osmosis. I recall a plant physiologist professor many, many years ago illustrating by sharing a story of being on a mountain road in a discussion with wife whether they were going uphill or not.  He claimed he got out of car, poured water on the road and declared that water runs downhill!  Water moves from a high concentration to a low concentration, such when diluted by sugar.  That principle applies to movement of minerals and compounds as well, if they can make it through barriers such as cell membranes.
 
Hormones are actively involved with movement of cell products.  Four notable groups of hormones are auxins, gibberellins, cytokinins and abscisic acid.  Each is associated with different functions in the plant.  
 
Auxins, such as indole acetic acid (IAA), affect cell elongation. Produced in the apical meristem it is associated with initial elongation of the stem tip.  Absence in the lateral buds at base of each corn leaf, prevents branching.  Removal of the apical meristem allows production of more auxin in lateral buds and consequential branching of the corn plant.
 
Gibberellins, such as gibberellic acid, promotes elongation of the cells in the stem but not in the apical meristem.
 
Cytokinins promote cell division in the meristems such as in the newly pollinated embryos.  Zeatin is a cytokinin in corn embryos.  
 
Abscisic acid inhibits cell growth.  It is most active in developing the restriction of flow of more carbohydrates into the mature grain, causing the cells at base of kernel to form a ‘black layer’.
 
It is not known completely how these hormones cause these affects.  It is mostly assumed that they are acting with cell DNA but some reactions, such as auxin causing roots of a germinating seed to turn to go downwards because cells on one side elongate more than those on the other side, seems too quick to only be reacting with DNA.  Regardless mechanism, plant hormones are essential participants in the communication among corn cells.

​Although many cells of the corn roots have the basic structures similar to other plant parts, there are significant differences appropriate to the root functions.  Root cell production originates from active root tips, producing epidermal cells, intermediate parenchyma cells and vascular bundles complete with xylem and phloem tissue. 
 
The important function of uptake of water and minerals occurs mostly through the youngest and newest cells near the root tips.  This is enhanced by extensions from some epidermal cells called root hairs, vastly expanding the exposure to the root surface for absorption that occurs mostly by osmotic pressure. This is enhanced by diluting the water in root hair cells with sugars supplied ultimately by leaves and transferred through the phloem.
 
Root hair cell walls block large items, such as fungal mycelium, but smaller molecules pass through to the cell membrane that is selective in allowing entrance.  Root hair extensions of the epidermal cells live for only a few days but as the root tip produces more new cells that produce new root hairs, the enhanced absorption of water and minerals continues.  Auxin hormones are involved in the initiation of the root hairs. The short life is probably useful as the permeability enhances the potential for invasion by pathogens.  After the root hairs disintegrate root cells increase the function of transporting to the xylem.
 
Of course, genetics influences the branching of roots, and production of root hairs. In addition to the multiple genes probably involved, a single root hairless mutant gene rth3 gene has been identified and in trials has shown to be associated with significant losses in grain yield. https://www.ncbi.nlm.nih.gov/pubmed/18298667/.
 
Lot of things happening in the corn plant that we don’t see.

​Xylem cells in the vascular system from the roots to the leaves is the main tube that allows water and minerals to be moved from roots to leaves.  A major portion of the xylem, tracheids, are dead cells at maturity that have strong thick walls providing the strength to withstand strong water pressures but have small pores to allow flow into surrounding cells.  Also, part of the xylem tissue, are living parenchyma that allow movement of water and minerals to other cells. These cells accumulate potassium ions to be distributed into mesophyll of leaves. Xylem parenchyma cells accumulate starches in the corn stalk pith areas, to be later moved thru the phloem vessels to the developing kernels after pollination. 
 
Tracheid cells in the xylem do not have end walls allowing them to form a tube.  Water pressure from water entering the root cells to the movement of water to leaves where a portion of it evaporates through open stomata openings, causing transpiration pull. This push and pull causes a constant flow of water through the tubes of the xylem.
 
Phloem cells provide the transport of sugar and protein molecules up and down the plants.  Xylem cells provide the flow of water and minerals up the plant.  Movement in the phloem occurs via living membranes and requires energy.  Movement of the water from roots upward does not require energy but simply removal of water through stomata and tendency of water molecules to adhere to other water molecules (cohesion).  Thick xylem tracheid walls form the tube to contain the force.

​Pores in cell walls allow movement of cell products between cells.  These pores are filled with an extension of the endoplasmic reticulum, the membrane-like filaments within a cell. This extension called the plasmodesmata is essential to plants because of the cell walls.  Animal cells do not have cell walls. These typically are large to move small molecules such a glucose but often need some energy dependent assistant to move larger ones such as proteins.  It is hypothesized that when some corn varieties are chilled the movement of the compounds from the chloroplasts in the leaf cells to the bundle cells adjacent to the veins for the final production of glucose is inhibited (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2958785).
 
Larger molecules such as RNA and proteins also move via plasmodesmata between cells with some specific chaperones’ molecules assistance.  This same type of assistance allows viruses to move between cells as well, eventually reaching the growing point to cause a systemic disease. 
 
Movement of carbohydrates from leaves to growing points, roots and corn stalks is facilitated with the plasmodesmata between cells of the phloem.  Hormones are also moved in the phloem to other plant parts by the same system.  Root cells also have plasmodesmata for hormone attraction of carbohydrates and proteins for growth.
 
Plasmodesmata represent another unique feature of plants, hidden from most of us, that is affecting the performance of the corn hybrid each season in our fields.