Plant cells have plastids, distinguishing them from animal cells. They are believed to have been derived from cyanobacteria, such as single cell blue green alga, when a symbiotic relationship with a single celled organism merged with it, perhaps a billion years ago. Like any symbiosis between organisms, each one benefits and they often become interdependent. Plastids, like bacteria, have two surrounding membranes and DNA organized in a circular manner as opposed to the chromosomal arrangement in all other organisms with a membrane-bound nucleus. Plastids multiply by division independent of host cell division but are carried along with new cells. Consequently, in corn, they are present in the female egg cell. After pollination, as the fertilized egg cell divides and ultimately forms meristems, each cell includes the plastids. These are called proplastids because they are not fully developed. Those in the cells reaching the light quickly are transformed into chloroplasts. Although plastids have their own DNA and capability to produced the many enzymes and other components of chlorophyll, as in other cases of symbiosis, they are also dependent upon the host cell to provide some proteins and plant hormones such as cytokinins needed for proper development.
A major structural feature of chloroplasts is formation of multiple layers of membranes (thylakoids) with the chlorophyll molecule and thereby enhancing the capacity for photosynthesis. The plant hormones classified as cytokinins, perhaps produced more by the host cell but some from the chloroplast itself, apparently affect the size and quantity of these layers. Host cell genetics, those inherited from both parents of a corn hybrid, thus influence the chloroplast development and function despite the fact that the proplastids are carried along in only the female parent egg cells.
All proplastids do not develop into chloroplasts. Those remaining below soil surface and some others do not become green and become sites for starch storage. Some others accumulate other pigments, contributing to other colors expressed in plants. Some chloroplasts located near the veins in plants develop slightly different carbon-fixing methods that allows corn’s photosynthesis to be among the most efficient of plants to convert light energy into carbohydrates.
Those corn seedlings, soon to be emerging in US fields, will have proplastids in coleoptile and other new leaves with newly-formed chloroplasts converting of light energy into the chemical energy needed for growth of the plants.
Within minutes of exposure to light, coleoptile cells, like other corn leaf cells, turn green, from chlorophyll production. This occurs within cell structures unique to plants called chloroplasts. These cell organelles, like mitochondria, are enclosed within their own membranes and have their own DNA. In fact, they have so much structure and chemical similarity to blue green algae (Cyanobacteria), chloroplasts are believed to have originated as a single event of a cyanobacterium gaining a symbiotic relationship within a single cell organism about a billion years ago.
Chlorophyll is a complex pigment that absorbs blue and red factions of light. A photon of light energy removes an electron from the chlorophyll molecule. This electron is transferred through a series of chemical reactions within the chloroplast until it ultimately ends up separating hydrogen from oxygen in water and combining hydrogen, carbon and oxygen molecules to make the carbohydrates for use elsewhere in the plant. Excess oxygen is released into the atmosphere.
Chlorophyll molecules are composed of carbon, hydrogen, oxygen, nitrogen and magnesium atoms. Genetics for the molecules is within the DNA of the chloroplasts and is inherited through the female seed parent of a hybrid. As the chloroplasts are exposed to light they are known to divide within cells and even to move within cells to become oriented to the light for best absorption of light. As an endophyte, they are dependent upon the cell for minerals and availability of carbon dioxide, but do produce their own enzymes.
Amazes me that as we see those green corn spikes emerging in the field, all of this is happening outside of our eyesight.
Elongation of cells in the mesocotyl pushes the corn seedling coleoptile towards the soil surface. Cells in the coleoptile are also elongating as it grows upward but cell function changes drastically when light strikes the emerging coleoptile. Meanwhile the immature leaves encased by the coleoptile are also slowly enlarging. Almost immediately after the coleoptile is exposed to light, hormones are produced that essentially shut down the mesocotyl growth. Other plant hormones, auxins, are produced in the shoot tips and transported to the node at the bottom of the coleoptile, stimulating the growth from root primordial cells to produce the secondary root system. Movement of this auxin in the opposite direction of the flow of water from the soil requires energy, as it must go from individual cell to cell. That energy is now being supplied by photosynthesis occurring initially in the emerged coleoptile and then by the new leaves that pushed out of the coleoptile enclosure. Previous to emergence, energy for growth was supplied by the seed endosperm and influenced by heat. Water supplied by osmotic pressure in the primary root tissue allowed for cell elongation in the mesocotyl. Now with exposure to light, a new source of energy moves the seedling to new phases of development above and below the soil surface. Mesocotyl significance to the seedling reduces as the above soil structures take over the physiology of the young corn plant. This transition does allow the plant to be vulnerable to negative temperature, moisture and pathogen affects but if everything goes right, the mesocotyl remains intact until the secondary roots function as the main supplier of water and nutrients for above ground growth of the seedling.
Interactions of host, pathogen and environment certainly affects corn seedlings. This will probably be emphasized this year in those western US corn fields that were planted and then covered with several inches of snow a few days later. Also, only 1 day after I blogged about how Fusarium species are often more or less innocent endophytes in corn seedlings, the most recent publication of Plant Disease includes a study showing a Fusarium species could cause corn seedling rot and one from China claiming another Fusarium species causing stalk rot. Both of these studies indirectly point out the difficulty of separating the environmental affect on the host from the pathogen aggressiveness. Simulating the field environment that a crop in the field really undergoes with laboratory conditions is problematic for all pathologists.
If a seed germinates at 60°F in moist loam soil, emerges in 7 days to sunny warm weather but is surrounded in the soil by fungi, some of which may penetrate the primary root tissue and may even progress between cells, causing the plant to produce the anti-fungal chemicals to restrict the fungus, is the fungus an aggressive pathogen of concern? How about if the seed was old with damaged mitochondria delaying emergence and having a weakened response to the invading fungus? Is the fungus now defined as an aggressive pathogen? Or, if the cold environment delays emergence and response time from the host to the invaders, is the fungus the cause of low plant stand? If the seed is planted in environment with high concentration of the fungus, causing the plant defense system to be overwhelmed, is the fungus now an aggressive pathogen?
It is not easy to separate the biology of the plant, complexity of environment and the biology of the potential pathogen when determining the cause of a corn emergence problem in the field. Usually it is related to each component of the disease triangle.
The fungal species of the genus Fusarium have a complicated relationship with germinating corn seedlings. The most studied species, Fusarium verticilloides (formerly known as Fusarium moniiforme and its sexual stage as Gibberella fujikuroi commonly is found in germinating corn seeds. It often is found in corn plants without symptoms of damage and therefore is characterized as an endophyte because it appears to live within the plant tissue but does not always cause symptoms. It is not uncommon to see growth of this fungus from germinating seed in paper germination test. A study published in 1997 (Plant Dis. 81:723-728) compared seedling growth from seed artificially infected with this fungal species with those that were not infected. There was no difference in germination percentage between infected vs uninfected seed. There was a slight size difference favoring the uninfected seedlings at 7 days after planting but at 28 days those growing from the infected seedlings were slightly bigger and with more lignin in cell walls. Is this because of a hormone (gibberellin?) produced by the fungus or because of some defense compound produced by the plant? The fungus was easily recovered from the seedlings but less from the older leaves. Infected plants showed no symptoms of disease.
It is clear that Fusarium verticilloides can be damaging to germinating seed sometimes but I don’t think all the factors are clearly understood. Is the difference caused by the strain of the fungus, the host plant or the environment? I know from experience that it is so common to find Fusarium growing from a dead leaf sample that one tends to ignore it. It seems to live in much of corn plant’s tissue. It often leads to confusion with diagnosis of problems including stalk rot, almost as if one cannot find other fungi usually associated with rotting stalks, there is always Fusarium. It’s complicated!
The mesocotyl is technically part of the stem tissue because it developed from the initial apical meristem in the embryo. As the seed imbibes water and begins germination, the cells of the mesocotyl begin to elongate. Individual cell growth was once described in a plant physiology class that I attended just a few years ago (Professor Loomis at Iowa State University about 56 years ago). He said it was like a balloon swelling with water. The cumulative affect of the cell enlargement pushes the rest of the stem tissue towards the soil surface. The leading tissue is the shield-like coleoptile. Cell elongation continues until the coleoptile is exposed to the red light component of sunlight. This stimulates production of a plant hormone that is transmitted to the mesocotyl cells causing them to stop elongating.
A few things can go wrong with this process. Temperatures influence the rate of growth of the mesocotyl cells, prolonging the exposure of the tissue to pathogens such as Pythium, a fungus that tolerates the lower temperatures. If the soil is not adequately compacted and thus allows light to penetrate, the stop growth signals come before emergence of coleoptile. If too compact, cell elongation is insufficient to push through. Growth regulating herbicides, combined with cold soils may cause the mesocotyl growth to stop. Cell elongation being dependent upon water for swelling makes the pushing of the coleoptile to the soil surface as well. Fortunately, all of these potential problems are rare, and the remaining development of the corn plant becomes less dependent upon the mesocotyl.
I did blog on 3/3/16 about corn germination testing but perhaps it needs to be addressed some more. It is a more difficult subject than would seem on the surface. Seed companies are required to state on the bag or box tag the germination percentage based upon a warm test and the month the test was performed. State laws may vary a bit but I think most require that the germination be done within 6 months of planting in the field. This requirement is good in that it provides some guidance to the grower and the seed company. There are some potential misleading aspects to this system. The seed laws also allow some variance due to sampling that, in reality, allows a warm test result of 89% to be legally tagged at 95%. Also, seed with a warm test result of 100% be labeled at 95% on the tag. The variance is necessary but it would be a disadvantage to the seed company and grower to have a 95% tag on seed that only had an 89% warm test, but it would be legal. I doubt that this is ever intentionally done.
The other enigma with the germination on the tag is that the warm test is usually not the best predictor of field emergence. Generally, the cold test is a better indicator of field emergence but the range of results among labs on cold tests is even greater than warm tests. Publishing cold test results by companies to the customers also requires a pretty long dialogue on the meaning. Throw into this mix the problem of adequately sampling a large seed lot and potential affects of damage in shipping and on farm storage on germination. Seed quality is one of the factors affecting plant emergence in the field. Studies of corn with acceptable range of germinations that I have seen over the years indicate that up to about 70% of the final stand in the field can be due to seed quality. Plant densities are only one of many factors influencing final grain yields. However, if reduced stands or uneven emergence did result in some yield loss, it may lead to the errant conclusion that the hybrid genetics were poor. Consequently, the grower switches hybrids for the wrong reason and the seed company has inventory problems the following year for the wrong reason.
We want things to be simple but that rarely is true when dealing with the plant biology and environments of agriculture.
Cell division after union of the pollen nucleus with the ovule nucleus in corn begins about 2 days after pollination. One of those two cells is destined to become the scutellum part of the embryo and the other the shoot and root. Over the next 45-50 days further cell division in the shoot portion results in cells destined to be the first 5 or 6 leaves and 2 layers of only a few cells at the tip that, although dormant from desiccation, remain as stem cells. These cells remain undifferentiated, that is not committed to any distinct plant part. This is the shoot apical meristem (SAM). With imbibition, water into the seed, cell division of these cells continues. Plant hormones such as cytokinins and gibberellic acid are involved in the rate and continual division of these stem cells at the tip of the shoot as it is near ground level while most leaves are now several inches above the surface. As the new cells do become committed to leaf tissue formation and axillary meristems with potentials to form ears.
Each corn cell includes a nucleus with the same 10 chromosomes and the same 32000 genes as the stem cells of the meristem but have become committed to produce specific tissue. Apical meristem cells in corn continue to produce more cells and resulting leaves and stem structure until special flowering hormones produced in the leaves are transmitted to the apical meristem cells to now produce those that become the tassel. That completes the life cycle of the apical meristem of corn.
This is how it works when all goes as we want. Some plant pathogens can interact with this system to mess up the plan.
Visit us at the ASTA in Chicago, Dec 9-12 (booth G207)
About Corn Journal
The purpose of this blog is to share perspectives of the biology of corn, its seed and diseases in a mix of technical and not so technical terms with all who are interested in this major crop. With more technical references to any of the topics easily available on the web with a search of key words, the blog will rarely cite references but will attempt to be accurate. Comments are welcome but will be screened before publishing. Comments and questions directed to the author by emails are encouraged.