​Emerging corn seedlings initially utilize the primary root for absorption of water and nutrients as this root tissue is powered initially by the endosperm and then the photosynthesis from the first seedling leaves. Initial stem nodes remain under the soil surface. Soil temperatures affect the growth rate of the seedling but by time the third leaf is visible inside the whorl of the seedling, lateral secondary roots emerge from the nodes below the soil surface. Photosynthate are moved to these root tips stimulating more cell in new root tips as hormones direct the growth down. Cells outside the dividing root tip cells develop a strong epidermis allowing the root to push through the soil.
 
Newly formed cells of the elongating roots, near the root tip includes epidermal cells with thin-walled protrusions called root hairs. These protrusions into the soil affectively expand the net root surface area of the root allowing flow of water and nutrients into the root by osmosis.
Cells in the core of the new root differentiate to form vascular tissue that connects to the stem vascular tissue through the nodes.  This vascular tissue allows transport of water and minerals upwards through the xylem and carbs downwards through the phloem. A few cells in this vascular portion of the young root maintain cell division capability, becoming stimulated by another group of hormones (cytokinins) to increase cells laterally, pushing through the epidermal cell layer becoming lateral roots with their own root meristems. As more lateral root branches form, along with their root hairs the water and nutrients shipped to the developing seedling leaves the upper leaves are formed and photosynthesis increased.
 
This early coordination of shoot and radical root emergence from the seed. Initially with energy from the seed endosperm and then from photosynthesis, allows the new plant to develop for its annual lifetime.
 

The initial roots growing from the embryo radical supply the emerging seedling with water and nutrients. Other changes then occur.
 
After the first corn leaves emerge, the hormonal message to the mesocotyl tissue is to stop pushing upwards. Apical meristem, at the tip of the mesocotyl is now below the soil surface where the first leaf is attached. Photosynthesis now drives the metabolism of the young seedling as it switches from dependence upon the seed endosperm for carbohydrates.  Cell division in the meristem produces new leaves, each attached to the young stem under the soil surface and attached in distinct clusters of newly dividing cells called nodes.  These nodes are then stimulated to produce roots at about the time the 4th leaf appears in the young seedling.  Because the roots are being produced from stem tissue, they are called adventitious roots.  As the primary root, that had grown initial seed, loses its energy source, adventitious roots become the main roots for the plant.
 
The first 4-5 nodes of the young stem remain underground, each producing the roots for the plant, even as the first leaves remain attached at the same locations.  What appears to be stem in a 4-5 leaf seedling is a compilation of leaf sheaths tightly wrapped together while the actual stem remains beneath the surface. The underground stem portion, formerly attached to the mesocotyl, with adventitious roots becomes known as the crown.  Eventually the mesocotyl deteriorates as it is deprived on nutrition and loses resistance to the many soil organisms.
 
As the stem growing point eventually emerges above the soil surface a few exposed nodes will often form the brace roots to further support the adult plant. A lot of changes in a relatively short time after seed is planted.

​As we look for those first seedlings poke up to reach the light it is easy to miss the amazing feat that has been accomplished. Breeder efforts is selecting genetics, seed producers care during production, and growers efforts with soil preparation and care in seed planting results in the biology of each seedling pushing the shoot up and root down. A cooperative effort by all results in a uniform emergence.

​The first appearance of corn seedling tissue emerging from the imbibed seed is the new root. This young seedling primary root can be considered as three regions: meristem, elongation and mature. The cell elongation area provides the main initial force for pushing through the kernel pericarp. Cell elongation and maturation involves production of many new molecules composing the cell walls as they grow. The pectins, hemicelluloses and celluloses that compose the new cell walls are composed of several sugar-related molecules joined together through specific reactions, assisted by enzymes, heat energy and chemical energy such as from ATP.

Energy and components for the biosynthesis of these cell wall components comes mostly from the endosperm. Starch in the endosperm is broken down with enzymes into sucrose molecules, moved to root cell cytoplasm where other enzymes break down the sucrose into glucose and fructose. With other enzymatic action, the fructose is made into more glucose. Modification of these sugars allows other new carbohydrate based molecules that become linked to form the more complex polysaccharides such as pectin, hemicellulose and cellulose for the new cell walls.

We see what looks like a rather simple process- seed swells, root protrude and a few days later the stem emerges from the seed. What we don’t see is a complex utilization of stored energy, production of complex proteins some of which act as enzymes assisting in linking molecules together and thus giving outer strength to cells. Also, unseen is production of anti-microbial compounds to ward off the many organisms attracted to the very molecules stored and manufactured in the seed. We don’t witness the genetics that programs for these processes. Humans successfully selected for these features from a wild plant species, adapting it to worldwide growing environments. The complexity of corn seed germination still can be challenged in a cold, wet spring such as being experienced in the central U.S.A. spring, but it is amazing that these processes work even under tough environments

​​Growing interest by corn growers in the USA to having seed tested for germination at temperatures typical of actual planting dates has resulted in several questions.  Many of these issues have been raised by seed producers for many years.  Why does some seed within a seed lot germinate and others not?  What causes some seed to not germinate under cold conditions although the warm test result shows they are alive?  What should be the minimum acceptable cold test result?
 
Hybrid corn is mostly bred to produce a large amount of grain per area of soil.  Most of that volume and weight is carbohydrate deposited in the endosperm. Genetics affecting the production and storage of carbohydrate is mostly biologically separate from the utilization of that stored carbohydrate into metabolism needed for growth of the plant.  A hybrid in which maximum grain production per plant occurs because the combination of genetics from a specific male and female parent are a match.  Those two inbreds, however, frequently differ in vulnerabilities to environments that affect germination.  The inbred that becomes the female plant in hybrid seed production becomes the genetic source of some cellular components such as the mitochondria and chloroplasts.  Mitochondria are especially significant in deriving the energy from carbohydrates to drive the metabolism needed for production of new cells during the germination process. This is probably the main biological reason that seed companies have identified certain parents as more reliable for germination.
 
Membrane systems, including those within mitochondria, are essential to cellular function.  Cellular membranes are also vulnerable to damage, especially during the rehydration after seed has be dried.  The damage is independent of temperature.  Movement of water through the pericarp into the embryo cells at the same rate in warm wet soil as in cold soil.  Sudden swelling of the membrane-bound organelles causes some breakage.  Remaining metabolism in undamaged portion repairs the damaged membranes.  This rate of repair is temperature dependent.  Repair is slower at lower temperatures.  If soil temperature is below 55°F, it is believed that very little imbibition damage to cellular membranes especially those of the mitochondria will occur.  In the field with low temperatures, the damaged seed and slow growth becomes vulnerable to invasion by microbes that can further inhibit seedling emergence.
 
Cold germination testing is intended to identify the percent of seed within a sample that have sufficient membrane damage to inhibit or delay germination and consequently not become a productive plant.  Developing reliable, repeatable test methods is a challenge resulting in multiple lab differences in results.  Some variability is due to subtle aspects of temperature of water, nature of germination media and definition of damaged seedlings usually called ‘abnormals’.  Added to the biological-environmental variables are the difficulties in adequately sampling. The initial source causing the imbibitional chilling damage vulnerability could have been disease or moisture stress in the production field, handling in the harvest, drying and bagging process.  Genetics, especially of the female parent also interact with all of these factors.  In many ways it is amazing that we produce mostly high germinating seed. (Corn Journal 4/24/2018)

​While we wait for the first signs of emergence from the soil with the coleoptile poking up to the light, the real action has been happening within the cells of the shoot and roots of the seed embryo. It is cell division and cell elongation that pushes the shoot tissue up and root down. That action is occurring as the cell organelles are activated

​It is difficult to imagine 32000 genes distributed among the 10 chromosomes in the nucleus of a single cell within the embryo of the corn seed. But the microscopic cell also contains many other substances that contribute to cell function once it is activated with germination. Proteins and lipids contribute to the function of the outer plasma membrane surrounding the cell, but membrane-like structures also are intertwined within the cells. Endoplasmic reticulum is used to transport cell products. Ribosomes are attached to the outside of ‘rough’ endoplasmic reticulum. These ribosomes are the organelles in which RNA codes, originating from the DNA, are used to link the amino acids to form proteins. Adjacent endoplasmic reticulum is used to transport the newly formed proteins to sites in the cell appropriate for that protein’s function.

Mitochondria, independent organelles within the cell, are the site of transferring glucose molecules in the chemical energy used by other cell functions. These organelles, carried along in the egg cell from the maternal parent plant, have their own DNA for genetics but are dependent on the rest of the cell and nuclear DNA to provide the glucose, proteins and lipids for structure and function. This symbiotic relationship is in all animal, plant and fungal species, originating a few billion years ago and certainly is significant in corn performance. Mutations in the mitochondria DNA are the source of cytoplasmic male sterility, at least partly because of a genetic defect in the outer membrane of the mitochondria results in defective pollen production. Integrity of the membrane of the endoplasmic reticulum, ribosomes, mitochondria, nucleus and outer cell membrane after imbibition of water is essential to that early activation of the seed embryo and the emergence that we anticipate.

​ 
Each seed in a single cross hybrid corn bag is slightly different in its biological and even genetic history.  Rarely are the two inbred parents in a seed field 100% homozygous plus some of those plants may have their own mutations.  Fortunately, drastic mutants are usually caught by the seed producer before pollination. An individual female plant in the seed field may produce 200-300 seed. And one 80000 kernel bag of seed corn must represent seed from 300-400 individual plants.
 
We want to think of all single cross seed in a bag are the same, but they are not identical genetically or in germination quality.  Even with multiple generations of selfing in development of the parent seed, some mutations occur with each generation of seed increase prior to planting in the hybrid seed field.  Most often these mutations are non-consequential to hybrid performance and especially not visible in the field where many small environmental effects are affecting appearance of the plants.  The closer we get to discerning DNA differences the more difficult it becomes to distinguish inconsequential differences from the drastic ones.
 
Seed quality differences among the seed in that one bag of hybrid seed also shows differences.  A warm test may show 95% germination but even beyond the non-germinating ones, there will be some that are slower to germinate than others even when all environment is uniform.   As the percent germinated gets lower, more late ones become evident.  A cold test, especially like ours at Professional Seed Research, Inc. in which we cover the seed with 3/4 inch of artificial soil, nearly always show lower percent germination and more late emerging plants than the warm test.  Why are all the seed not with the same quality when produced in same field?
 
Unfortunately, not all the seed on a single seed field ear have the same environment. First silk, coming from the ovules near the base of the ear, emerge 3-6 days before the final silk.  Successful pollination by the correct male parent is dependent of many variables, including factors associated with maturity for the male and female in the seed field.  In general, pollen timing is affected more by accumulation of heat units whereas silking is favored by water.  Cool wet pre-flowering weather can lead to silks being exposed before pollen.  This not only makes the seed more vulnerable to contamination by outside pollen from field corn, resulting in outcrosses, but also to infection from fungi such as Fusarium or Diplodia species traveling down the silk channel before it closes after pollination.  The opposite can happen with hot dry weather, in which the silk emergence is delayed, causing the pollen to be spent before all the silk emerges.  Consequently, there often are differences in germination (and outcrosses) among seed positions on the ear.  

We humans have adapted a tropical plant (Teosinte) and created a species adapted to temperate zone called Zea mays. Along the way, selections were made to allow germination of seed and early growth and at very non-tropical, low temperatures. It also requires careful seed production, storage and planting.

Hybrid corn is mostly bred to produce a large amount of grain per area of soil. Most of that volume and weight is carbohydrate deposited in the endosperm. Genetics affecting the production and storage of carbohydrate is mostly biologically separate from the utilization of that stored carbohydrate into metabolism needed for growth of the plant. A hybrid in which maximum grain production per plant occurs because the combination of genetics from a specific male and female parent are a match. Those two inbreds, however, frequently differ in vulnerabilities to environments that affect germination. The inbred that becomes the female plant in hybrid seed production becomes the genetic source of some cellular components such as the mitochondria and chloroplasts. Mitochondria are especially significant in deriving the energy from carbohydrates to drive the metabolism needed for production of new cells during the germination process. This is probably the main biological reason that seed companies have identified certain parents as more reliable for germination.

Membrane systems, including those within mitochondria, are essential to cellular function. Cellular membranes are also vulnerable to damage, especially during the rehydration after seed has be dried. The damage is independent of temperature. Movement of water through the pericarp into the embryo cells at the same rate in warm wet soil as in cold soil. Sudden swelling of the membrane-bound organelles causes some breakage. Remaining metabolism in undamaged portion repairs the damaged membranes. This rate of repair is temperature dependent. Repair is slower at lower temperatures. If soil temperature is below 55°F, it is believed that very little imbibition damage to cellular membranes especially those of the mitochondria will occur. In the field with low temperatures, the damaged seed and slow growth becomes vulnerable to invasion by microbes that can further inhibit seedling emergence.

Cold germination testing is intended to identify the percent of seed within a sample that have sufficient membrane damage to inhibit or delay germination and consequently not become a productive plant. Developing reliable, repeatable test methods is a challenge resulting in multiple lab differences in results. Some variability is due to subtle aspects of temperature of water, nature of germination media and definition of damaged seedlings usually called ‘abnormals’. Added to the biological-environmental variables are the difficulties in adequately sampling. The initial source causing the imbibitional chilling damage vulnerability could have been disease or moisture stress in the production field, handling in the harvest, drying and bagging process. Genetics, especially of the female parent also interact with all of these factors. In many ways it is amazing that we produce mostly high germinating seed.

​Each plant of a single-cross hybrid has the identical genetics, including those affecting the speed of seedling growth.  Uniform seed quality and environment will allow uniform environment. Hybrids differ in the speed of emergence but uniformity of emergence within a field becomes an important component of maximum grain yield.
 
Corn embryo’s being planted on May 1 are about ¼ inch (0.6 cm) in length. The future shoot portion of the embryo is half the size of the embryo. Two to three months later that shoot length has been multiplied by 800-1000.  Within the embryo are cells with organelles such as mitochondria, plastids, ribosomes and other membranous structures needed to carry out this remarkable growth rate. Within the nuclei of these cells are the 10 pairs of chromosomes with the 30-40000 genes, coded by long strings of nucleic acids.   Within a few hours of water imbibition, the few genes in the mitochondria are activated. Appropriate codes within their DNA produce RNA strings of nucleic acid, that are moved to ribosomes, producing proteins appropriate to enzymatically remove the energy binding the carbon and oxygen molecules in glucose and moving that energy into adenosine triphosphate (ATP).  This energy is utilized in manufacturing the other structures for rapid cell elongation and cell duplication, pushing the seedling shoot to the soil surface.
 
With exposure to light, some cellular plastids with guidance from their own DNA and supplies from the other cell components, produce chlorophyll. This pigment allows absorption of light frequencies providing energy to drive the capture of carbon, oxygen and hydrogen molecules in the process of photosynthesis.  Resulting glucose molecules are moved to the growing cells that utilize the new molecules in manufacture of structural complex molecules such as fatty acids and proteins used for cell metabolism and cell wall structures such as cellulose and lignin.

 
It is easy to be amazed when we seed the rapid growth of young corn plants and even more impressed to know that we are only seeing the result of remarkable interactions occurring at the cellular level.  
 

​I find it interesting to realize that much of what we see in a corn plant from germination to maturity is happening out of the sight of most of us. After germination, the root shoot heads downwards and the shoot grows upwards, regardless of orientation of the seed in the soil. Plant hormones auxins, cytokinins and gibberellins are primary in affecting growth directions of these tissues. Those interactions are affecting the cell growth in those tissues, especially whether they elongate or not. The affects do not really end with germination.

Cytokinins and auxins are operative during all of the corn plants life, including the movement of sugars to the young kernels. These two kinds of hormones have different roles in origin and effect on corn growth. Cytokinins are mostly produced in root tips in root meristems and transported through the water distribution in the xylem tissue. Auxins are mostly produced in stem meristems and distributed in the phloem system. Cytokinins are associated with increasing cell division in the stem meristems whereas auxins are involved in cell elongation. Apical dominance resulting in the corn plant usually having only one upright stem is because of the interactions of the auxins produced in the apical meristem. Removing that stem tip in early corn development and thus reducing auxin production tips the balance towards more cytokinin and stimulation of cell division in the lateral buds of the corn plant, resulting in branches.

Pollination of the multiple ovules in the corn ear results in attraction of cytokinins to each developing kernel. Moisture stress during the first 10 days after pollination is known to cause early death to some kernels, perhaps because of reduction transportation of cytokinins to the most immature embryos (my conjecture!). Cell division in the new embryo meristems establishes the movement of sugars through the phloem to the kernels. Much of the sugar is deposited into the endosperm portion where it is changed to more complex carbohydrates and thus allow the osmotic pressure for more sugar movement towards the kernels.

More is known about the effect of these plant hormones on plant growth than all of the mechanisms involved with those effects. Auxins involvement in cell growth involves softening cell walls, making elongation of cells easier. Cytokinins have been shown to prevent protein breakdown and activating protein synthesis.

Cytokinins produced in root meristems are transported to and stimulate the cell division in the kernel embryos. Meristems of those embryos produce auxins. Auxins are associated with production of ethylene which has been associated with formation of abscission tissue as leaves and fruit mature. It is assumed that the auxins are associated with formation of the black layer at the base of kernels, resulting in stoppage of movement of material to the kernels.

We know that these plant hormones are associated with the growth of corn tissues including the formation of kernels but there remains lots to learn of the actual molecular interactions that allows this to happen. Meanwhile, corn breeders, agronomists and growers attempt to coordinate it all by selecting the genetics that maximize grain production. AND, new knowledge is coming as those interested in the science continue to research into the processes that most of us witness but don’t see the minutia at the cellular level.

​Corn seed is planted in complex environment with a mix of soil particle density, moisture levels and other organisms, some of which capable of digesting any carbohydrates they can reach. When seed does not emerge as expected we often look for a cause including fungi associated with the poorly emerging seed. This often is not simple.

Among the perplexing interactions in corn is that with corn and the fungus Fusarium verticilloides. This fungus was formerly known as Fusarium moniliforme and is the asexual stage of the fungus Gibberella fujikuroi. Many, (most?) seed samples germinated by paper methods will show at least a few seeds with this fungus growing from them, even with the appearance of normal seed germination. The fungus does produce a toxin called fumonisin that can cause rejection of grain by some livestock and grain elevators. This can occur in kernels showing not symptoms of infection.

The fungus can be found in corn roots, stalks and leaves as well, often without symptoms. It is not unusual to find this species growing from dead corn leaf tissue when moistened. It is as if it is an inhabitant of corn. Does it become transmitted to the next generation from infected seed? It is acknowledged that seed can be infected via growth of the fungus in the silk. Or does it become from infected debris in the soil? Or, perhaps entering thru injuries to plant tissue.

A study published at Appl Environ Microbiol. 2003 Mar; 69(3): 1695–1701 followed the spread of F. verticilloides from infected seed and from inoculated soil through corn plants using a carefully designed group of experiments using fluorescent strain of the fungus detected by fluorescent microscopy. They confirmed that this fungus can infect through the root to the mesophyll, often growing between cells. This can result in stunted seedlings, especially if grown under low light conditions. This growth can advance into the stalk tissue, in leaves and even into the seeds, sometimes without showing symptoms. More of the fungus was found in the plant if the soil inoculum load was increased. There was spread to the roots and to the rest of the plant from infected seed but the soil inoculum load appeared to be more significant.

Low light association with increased symptoms suggests that the metabolic health of the plant affects the defense against this fungal invasion. That also is consistent with the presence of this fungus in nearly all rotted stalks. If other stalk rotting fungi, such as those associated with Diplodia stalk rot, Gibberella stalk rot or Anthracnose stalk rot are not found, we tend to call it Fusarium stalk rot because it is always there. The low physiological state of stressed corn plants as they approach completion of grain fill increase the vulnerability the expansion of this fungus into the dead stalk tissue.

Microbes inhabiting the corn plant reflect the complexity that actually is affecting the biology of the corn plant.

​As corn seed is moved from a dry environment of storage encouraging slow metabolism to the wet, more complex environment of moist soil, germination and emergence becomes our next measure of success. 
 
It is difficult to sort out the real cause of seed not emerging or emerging much later than adjacent plants.  Seeds are planted in environments that vary every few inches for water holding capacity, organic content and microbes.  Furthermore, each individual seed varies slightly in its cellular membrane status.  With imbibition causing swelling of the membrane bound cell contents, some seed can have problems getting effective metabolism for early cell growth to push out the root and stem structures.
 
Cell metabolism includes producing the response to attacks by potential pathogens in the soil. These anti-pathogen chemicals (phytoalexins) are usually produced with a complex system of detecting the microbe and concentrating the phytoalexin into the area of the attack.  Weakened seed not only are likely to release more carbohydrates and proteins into soil because of membrane injury, but also be less capable of responding to the microbes invading root and mesocotyl tissue.
 
Diagnosis of seedling disease becomes complicated also.  Pathologists can isolate a fungus such as a Fusarium species or an oomycete like a Pythium species, but the actual cause probably involves some interaction between the microbes, metabolic quality for the ‘diseased’ seedling, and a complex environment not only providing potential pathogens but also affecting the seedlings metabolic rate. Soil organisms are affected by the environments as well.  Leakage of carbohydrates directs their growth toward the seedling roots but temperatures favor some over others.  Pythium’s swimming spores do well in cool wet environments but can be inhibited by certain seed treatments that have very little effect on fungi such as Fusarium species.  Other seed treatments can inhibit the latter group of microbes but are less effective against Pythium.  Corn seed genetics and seed quality can be greater factors than either group of chemicals.  Cold wet heavy soils for a prolonged time can overcome all methods of defense.
 
After the stress on the seedlings is reduced, remaining plants that emerge can give normal production especially if they are uniform in growth with adjacent corn plants.  The metabolism of these plants will promote the recovery and normal root growth.  Those plants that survive but emerge later than adjacent plants will have difficulty competing for light and mineral uptake which will be reflected in grain productivity.
 
Life for the corn plant, like for the rest of us, becomes more complex after we start living in our environments.
 

​Upon planting seed is exposed to an environment with many factors affecting the success of germinating and successfully producing a growing plant.  When corn seed, with its own biological potential problems, is placed in soil populated by multiple micro-organisms ready to feed on organic matter, multiple battles begin.  As the seed imbibes water, internal membranes swell, causing some leakage of stored sugars and proteins into the soil.  Many soil organisms grow towards the damaged seedlings, attracted by the leaked substances.  First tissue exposed to the potential invaders are the primary root and mesocotyl, two tissues that are later disposed when the secondary roots take over for the main root functions.  Invaders are detected chemically by the corn cells near the invasion, turning on local production of resistance antibiotics.  Success in suppression of the invaders is affected by aggression and intensity of the potential pathogens, environmental effect on pathogens and seedling and the biological vigor of the seedling.
 
Several fungal species are associated with seedling root rots.  Fusarium, Penicillium, Pythium and Rhizoctonia species are among the most prominent fungi found in diseased corn seedlings.  Fusarium species are common in nearly all soils with any organic matter.  Every corn seedling is exposed to this fungus and yet only a few show symptoms. The actual cause of the seedling disease is usually more complex than simply identifying the fungus present in the corn tissue.  Analysis of the cause should include consideration of environmental factors such as water concentration and temperature, and seed germination quality.  Vigorous seedling growth can quickly dispose of primary root and mesocotyl dependency as secondary roots develop and new leaf tissue produces the quantity of resistance factors needed to control potential invaders such as these fungi.
 
Seed treatments can give the seedling some temporary relief from fungal invasion pressures.  Genetic variability within the pathogen population can weaken its affect in some circumstances.  Vigorous early growth due to corn hybrid genetics and seed quality favor escape from seedling disease pathogens even when environments are not optimum for early corn growth.  Corn genetics and seed viability tests are strong deterrents to seedling diseases.  Favorable environments also contribute.
 

45 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 (Seedling Growout® test).
 
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 plants in the field compete with each other for light, nutrition and water.  Although genetically identical, this small disadvantage of the late emerging plant can detract from the final yield in the field.

I am amazed when I see our grandchildren move with seemingly little effort.  Did I ever move that way?  Sadly, we do age and and it is not only in our minds but in all cells of our body.  The speed in which seed and us age is influenced by our genetics, and environments after our 'birth'.
​
The mechanisms between us and seed may be similar in that mitochondria are probably involved in all deteriorating living cells.  These organelles which can number a few hundred in a cell, are the main sites for transformation of stored carbohydrates into useable energy for other cell functions.  Mitochondria have their own DNA and are composed largely of membranes.  Dehydrated seed results in mitochondria functioning at a very low level resulting in being unable to repair deteriorating membrane structures.  While at very low kernel moisture levels (6-14%?) and cool temperatures (less than 50°F (?) further damage is limited.  Precise moisture percentage and temperature for best storage of maize seed probably varies for genotype and seed condition but the general concept remains.
 
Seed imbibition of water is a physical phenomenon with little inhibition from the pericarp or seed coat.  Seed treatments added to seed can slow down the imbibition, apparently giving the renewed mitochondrial function more time to repair damaged membranes.  On the other hand, only increasing kernel moisture slightly can cause more membrane damage to occur, but not repaired.  Increasing moisture more while at low temperatures (50°F) has the same effect.  Corn seed planted in cold soils will imbibe water, but the low temperature inhibits normal cell function, including repairing mitochondria.  Those individual seeds with the most mitochondrial damage are likely the ones that struggle to germinate when the soil temperatures do heat up.
 
Seed producers are aware of the significance of inadvertently adding a small amount of moisture, such as from a seed treater before bagging by designing their process to limit the water and allowing for drying after application.  I recall a case in the Thailand in which a new fungicide seed treatment was applied to control downy mildew, but the humid environment did not allow the seed to dry after application.  Seed germination quality quickly deteriorated as a result.  Accelerated aging test of corn seed is based upon placing seed in an environment of 100% humidity and 113°F for 3 days, then planting in germination test to record the reduced germination.  It is intended to predict the viability of the seed after storage.  It is notable that even under this condition, all seed within the sample are not equally affected.  Some germinated normally, some eventually and some not at all.  This is typical of normal, well treated aging seed lots.  Each individual seed is in a slightly different condition.  We expect maximum performance when emergence is uniform.  

​Energy for germination of a corn seed not only comes from stored carbohydrates but also from surrounding environment.  Heat energy is a major contributor.  Although imbibition is not inhibited by cool temperatures, heat energy allows the orderly repair of the membranes damaged during the dehydration of drying seed and then the hydration after planting. 
 
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.

 ​Corn seed planting time is approaching in the northern hemisphere. The processes of successful producing and storage of the seed will soon come to fruition.  The selection of seed parents, care in the seed field of the last season and then the drying, shelling and storage all have an affect on reaching the goal of getting a uniform emergence in this next stage of growing corn.
 
Cells in a developing embryo are sufficiently mature to germinate in only 15 days after pollination if separated from the endosperm.  Early germination (vipipary) is inhibited by the presence of the plant hormone, abscisic acid, in the endosperm which negates the growth stimulant hormone, gibberellic acid, in the embryo.  This allows normal seed desiccation as water is replaced with starch deposits and eventual seed germination inhibition because of low water content.  Seed producers know that each genotype differs in the percent moisture to be used to harvest for optimum seed quality.  Generally, for most corn dent hybrids, that moisture is higher (+/-36%) than normal black layer moisture of 32%.  From there the moisture level must be rapidly decreased to less than 13 % to prevent excessive aging caused by damage to the cell membranes.  It is the art and science of the seed producer to bring the moisture down rapidly without using excess heat which also could damage the membranes.
 
Intactness of the pericarp affects the speed of imbibition of water in the soil.  Allowing the membranes surrounding each cell as well as the cell internal membranes to swell back to normal size with minimum injury is essential to their functions.  Cell membranes being the main structural component of embryo cells needed for energy conversion from starch in the mitochondria and translation of DNA to proteins, have a major effect on the germination quality of seeds.  Genetics of mitochondrial membranes, at least partly affected by the mitochondrial DNA, are probably one of the major reasons that seed quality varies between hybrid parents.  Mitochondria of the seed are replications of those in the female parent.  This is the major reason why choice of which hybrid parent becomes the seed parent.
 
Another major factor affecting on seed quality is the growing environment in the seed production field.  Stress, from drought or disease during the seed maturation period shows later in seed germination quality.  Such seed often becomes evident in germination tests done 4-5 months after seed harvest, sometimes in contrast to tests done only a few months earlier.  It is as if these seed had some membrane pre-harvest injury that when added to normal aging during these 4-5 months surpassed the minimum for normal germination.  These individual seeds either fail to germinate or are slower to emerge than other seed in the same seedlot.

Not only is our species dependent upon diversity for survival as our environment, including pathogens, changes.  We are depended upon diversity among our crops as well.  Corn being naturally cross-pollinated and diploid provides this opportunity for the diversity that comes from naturally occurring mutations.  It is basic to providing the eventual variability that has driven and continually drives evolution.  It allowed the deviants in Teosinte that was selected by people in Mexico 10000 years ago and the multiple selections in corn as it was moved worldwide since then.  Most research has verified that most of these genetic mutations result in recessive genes and thus the presence of the mutation is not often expressed in a diploid present in which the dominant member of the paired gene is expressed. The su genes resulting in sweet corn is only expressed when the recessive gene is expressed in both members of the diploid plant.  Same is true of the mutants wx for waxy.  This is true for multiple other homozygous recessive traits.
 
Occurrence of mutations can be an advantage or a disadvantage.  In most cases, being recessive, the mutation may not be detected by performance of the hybrid.  Selfing to achieve homozygosity during the inbred development reflects the negative affect of making some recessive genes more homozygous.  This is reflected in reduction of plant size from the heterozygous parent used for inbred development. The selection process with each generation does allow elimination of some negative homozygous recessives.  Double haploid systems do not allow generational selection because the homozygous condition is fixed.
 
Expression of hybrid vigor when an inbred is crossed with another specific inbred is mostly due to dominant versions of the negative recessive genes of the inbred parents.  That is probably why prospective commercial hybrids are from crosses of inbreds with distinct ‘families’, each not likely to share the same negative recessive versions of important genes.  Corn has 40000 genes, including some negative recessives, perhaps due to mutations.  The seed industry uses hybrid testing, and inbred development to select for hybrid performance.  Further selection among those near-inbreds can allow for selection against the few negative traits found among some plants to improve inbred performance in hybrid production.  That has been consistent with our experience in our proprietary Rapid Inbreeding® program.  Diversity is good!

​Opportunities for mutations occurs with every cell division but those that really count are those that occur during meiosis, in which all cells dividing from the fertilized egg cell will lnclude the new DNA arrangement for that segment of the chromosome.
 
​Corn advanced from that first mutation in Teosinte, allowing and exposed kernel to be easily used as grain.  More mutations that occurred with each annual reproduction was utilized by people over the past 9-10000 years.  Mutations occur naturally in all organisms. For example, each new human baby, on average, has 100-150 new mutations different from either parent.  Majority of the human mutations are unnoticed and insignificant but a few can be drastic.  But human generation reproduction is once every 20 years whereas an annual plant such as corn produces new mutants with each seed generation.  Although the mutation rate per gene may be low in comparison with some organisms, having 32000 genes allows for a probability of some mutations to occur with each generation.  Not all of these mutations will be expressed because they will usually occur in one strand of the paired DNA strands, allowing the other dominant version of the gene to affect the trait associated with the gene.
 
Mutation causes are associated with errors that can happen during meiosis and recombination of gametes during reproduction.  Point mutations occur when a different nucleic acid is substituted during DNA replication. This small change can code for a different amino acid when placed in the eventual protein produced from the DNA-RNA-protein process.  This can lead to a difference in some biochemical process that the original protein, acting as an enzyme, would affect.  It may affect drastic and very visible differences in the plant but in most cases, it is insignificant and not noticed by most observers. Point mutations are probably the most common cause of mutations but a few other more drastic causes can be related to major errors in DNA duplication as part of meiosis. It is common, however for some breakage in one of the pair allowing a segment to be exchanged with a portion of the member of that pair.  This process, called a crossover, is utilized by corn breeders in backcrossing procedures in which the objective is to cross a specific gene, such as a BT gene, into a desirable inbred without disturbing most of the genetics of the original inbred. Backcrossing in a gene, long used as a breeding procedure before use of GMOs, has been relatively successful in recovering the essential genetics of the original inbred but now with the desired gene such as the Ht gene for resistance to the fungus causing northern leaf blight or wx (waxy corn gene).

​Corn growth is done by enlargement of cells, often with the assistance of water pressure before the cell walls have solidified and by cell duplication.  Cell division is is a remarkable process that first requires the duplication of the chromosomes within the nucleus by a process called mitosis.  This delicate process should result in exact duplication of each chromosome pair, followed by new membranes forming around each set of 10 chromosomes.  This process is called mitosis is nicely described and illustrated in https://www.nature.com/scitable/topicpage/mitosis-and-cell-division-205.
 
This process is not mutation proof.  During the chromosome duplication process a segment of a DNA string may not reattach properly, resulting in an important expression of a trait to be changed or missing in the resulting cells.  Because this new cell and other cells duplicated from this mutated cell will likely contain the same mutation it may become evident to our eyes like a long non- pigmented streak in a corn leaf.  Most such mutations are hidden from our eyes and have minor affect on the plant performance.
 
Mitosis in a corn plant occurs mostly in the root and shoot tips from the embryo stage completion of shoot and tassel formation.  Another remarkable process occurring mostly out of site in the corn field.