The chemical warfare between the host plant and pathogen occurs without much of our attention.  Differences in resistance to different pathogens among corn hybrids can be visible and we attempt to characterize these differences but the cellular interactions have required careful lab studies.  Plants preserve energy by delaying the pathogen defense until the pathogen has invaded.  With fungi, the initial reaction is to a common component of nearly all fungal cell walls (chitin).   With that detection, signal hormones, such as salicylic acid is produced.  The fungus produces enzymes to attack the host cells, as the signal hormones activate the resistance genes to produce the proteins to limit the fungus.
 
Most corn pathogens feed on the dead cell tissue, even after the progress of the pathogen in the leaf tissue is stopped.  From the limited, dead tissue the fungus produces spores and spreads to fresh leaf tissue on the same or different plants.
 
A few corn pathogens, however, can only reproduce when feeding on living cells.  Smuts and rusts are these sort of pathogens that are called biotrophs.  These fungi invade living cells without killing the cells, while feeding on the cell and then spreading to adjacent living cells.  Resistance to this type of pathogen can involve a single gene system in which the host plant detects the presence of this type of pathogen and then produces the signal molecule at such concentrations that the host cell dies and, consequently, so does the pathogen, stopping the spread of the pathogen to adjacent cells.  This resistance system is generally inherited by a single gene so genetic diversity in the fungal population often includes single gene mutant variants (races) that overcome this sort of resistance system.  Common smut fungus (Ustilago maydis) includes a race that produces an enzyme that digests the signal molecule salicylic acid before it can cause the host cell to die and therefore the fungus now can spread to adjacent cells. Single gene resistance to rusts for many crops, including corn, are commonly overcome by single gene differences in the rust pathogen that suddenly makes a variety susceptible. Genetic diversity works for both parties.

Corn plants now (June 28) in much of the US corn belt are stretching upwards, for the most part showing little signs of stress.  We have little cognizance, however, of the internal battles that are going on in each of those plants. All plant parts are exposed to potential invaders, through injuries, through stomata or other openings and through direct enzymatic attack from pathogens outside the plants.  Plants have systems to fight the invaders by responding with anti-microbe chemicals or even initiating cell death to limit the damage. 
 
One of the key components of that mechanism is salicylic acid. This chemical was known by Hippocrates about 2400 years ago in an extract from willow bark that could relieve humans with headaches. Yes, it is the main component of aspirin.   Salicylic acid production in plants increases when cells are stressed from pathogens, drought, or toxins.  It functions as a signal molecule, triggering the production of a series of proteins to limit the damage.  Of course, the response time for salicylic acid production and consequential protein production to stop the potential pathogen is dependent on the plant genetics and nutrition.  Pathogens, no slouches in evolution either, often include mutations to slow down the production of salicylic acid by either tying up its component compounds or interfering with the production of the resistance compounds.  It’s a battle out there!

It must be human nature to try to make complex things into simple.  We see this in politics, economics and probably many aspects of human relations seem to want it simple, even if it isn’t.  Those of us that have studied corn and its diseases and certainly anyone growing a corn crop know that the actual environmental interactions with the crop is complex but we still are inclined to try to simplify the interaction between a microbe and the corn plant.
 
In reality, corn roots are invaded by a variety of fungi and bacteria, some of which simply live off of plant products and don’t cause any visible harm to the plants.  Some would call these organisms as endophytes (living with plants but not causing damage). 
 
Presence of these may be detected by the host plant, causing it to produce compounds that restrict the growth of these endophytes into more active plant cells.  In some cases, this appears to restrict more active pathogens.  Species of the genus Trichoderma have been noted as a type of biological control, but also some studies have noted fungal species of Fusarium, Acremonium, Aspergillus, and Botryodiplodia have similar interactions with corn.
 
It becomes more difficult to classify organisms that may once be a harmless endophyte but later, perhaps as the plant begins senescence either because of age, stress or simply shortage of adequate products of photosynthesis in some tissues. Cells in these areas perhaps cannot produce the resistance products needed to stop the foreign organism from killing weakened host tissue.  Do we now designate the organism as a pathogen? 
 
Often it is easier to name a disease, implying that an aggressive pathogen attacked the plant is appealing. Often, however, looking at the more complex aspects that allowed the organism to attack the plant could help avoid the repeat in the future. With many plant physiology, environmental and micro-organisms dynamics it is difficult for research as well as to adequately and completely describe.

 
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 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.
 
Meanwhile some pathogens, such as Sclerophthora macrospora, cause of crazy top of corn, that probably reached the growing point at the V1 or V2 stage is carried along, thriving on the movement of corn carbohydrates being moved to the tassel and ear shoots. Viruses, usually carried to the growing corn plant by insect vectors move through the phloem tissues in the direction of carbohydrate flow. Various resistance systems can ward them off but susceptible varieties can be damaged greatly.
 
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.

Corn at the V6-V8 growth stage has an excellent infection chamber, the leaf whorl.  This ‘cup’, even in the driest conditions always has some free water due to transpiration in the newly developed leaf tissue.  Although growth pushes the current moist tissue into the drier atmosphere with 12 hours, this is enough time for many fungal pathogen spores to germinate, hyphae to set up their drilling stations (haustoria) and enter the leaf tissue. Evidence shows in the formation of a group of yellow spots in leaf tissue a few inches from the whorl as the plant reacts to the invaders.
 
Rust spores often move to the Midwest on upper winds, initially from the southern overwintering location and then move further by more local winds as they produce spores in other infected fields.  More local fungi, such as Exerohilum turcicum, cause of Northern Leaf Blight, and Bipolaris maydis (Southern corn Leaf Blight) or Bipolaris carbonum (Northern Leaf Spot), often produce spores on moist, infected debris from the previous years that move to the moist whorl, quickly penetrating the leaf before it becomes dry.  Yellow spots are seen within 48 hours.  Typical Northern Leaf Blight lesions are not seen for two weeks but then generally in a band across the leaf that was in the whorl when this infection occurred.  Further spread of the disease depends upon showers allowing for exposed leaf tissue to have a moist surface for spore germination and fungal penetration.
 
Those yellow spots represent the beginning of the plant’s reaction to the pathogen.  Host genetics affect how successful the plant is in preventing further spread of the fungus. 

Several fields in Northern Illinois have ponded areas that have been replanted after the first plants were drowned.  There are also seedlings in some fields in some parts of the northern belt that are dying in fields, some clearly infected with Pythium species.  They grew from treated seed.  There have been reports of strains of Pythium overcoming most common seed treatments but it is notable that many seeds were in cool wet conditions for 3 weeks before emergence.  Did the seed treatment lose effectiveness over time?
 
Reports of Southern Rust in Louisiana reminds us of the corn crop vulnerability to Southern and common rust diseases during stormy June weather patterns.  Puccinia polysora (Southern Rust) and Puccinia sorghi (common Rust) overwinter primarily in the Caribbean and Mexico areas before blowing north east with storms.  Spores carried by wind that dump into the open whorls of young plants germinate in these moist chambers. Germinating spores quickly invade the cells and within a week pustules show up a few inches up on the new leaves in a band, indicating when the spore shower occurred. These become the inoculum source for spread elsewhere within the field, hybrid resistance and and weather for the rest of the summer determines the rest of the disease development.

Sorry for delays in recent posts.  I thought appendectomies were for teenagers but I guess I was wrong. Hopefully back on track next week.

Lateral roots are initiated from primordial cells in epidermal cells close to the root tip of secondary roots.  Not all primordia cells, however, further develop into lateral roots.  Environment factors such as soil moisture and genetics influence triggering the primordia’s cell division and setting up lateral root tips.  The more lateral roots, the less carbohydrate available for growth for the secondary roots.   Each lateral roots requires energy for growth, resulting in shorter roots.

​There is some evidence that more lateral roots favor phosphorus uptake because this mineral tends to not be mobile and that nitrate uptake tends to be favored by fewer laterals because this mineral is more mobile. This becomes especially significant when either mineral has a short supply in the soil.
(http://www.plantphysiol.org/content/166/2/590)
 
Root tips from the laterals and main secondary produce the auxins that attract the carbohydrates to the roots, allowing root development. Absorption and movement of water and mineral to the stem and leaves allows larger leaves and consequently more carbohydrate production.  Being underground we still do not know everything about root development but it obviously depends upon lots of variables, some of which we control.