organic is the new conventional

Organic spinach has a big problem — downy mildew. Conventional growers have effective sprays for it, but organic growers rely largely on resistant spinach varieties. Unfortunately, new races of downy mildew that overcome spinach resistance genes are appearing every year.

Downy mildew is not a true fungus, but an oomycete, a relative of the potato late blight pathogen, the one involved in the Irish potato famine. There are hundreds of species of downy mildew, each specialized on one or just a few host plant species. Spinach downy mildew is not known to infect any other plant species besides spinach. The pathogen grows inside the leaves, causing them to yellow and wilt, and then it emerges from the stomates on the underside, giving a characteristic downy appearance. The soft downy portion produces spore-bearing structures anatomically characterized as sporangia (singular sporangium) that themselves break off and float through the air, acting as individual spores to propagate the pathogen.

Downy mildew is a problem not just for its direct effect on spinach leaves. Because organic spinach from California once had an instance of E. coli contamination that sickened many consumers, killing three, any infection of spinach is looked upon with suspicion by wholesale buyers, even that of a pathogen that cannot infect any plant but spinach, much less a human. Thus the threshold for rejection of an entire field of spinach is 1-5% infection with downy mildew. This low rate may help reduce the chances that a clamshell of spinach will turn to mush, but it makes organic spinach production a risky endeavor.

Dr. Robin Choudhury did his dissertation research examining the disease dynamics of spinach downy mildew. He studied aerial spore (sporangium) dispersal by means of traps with small sticky rods revolving around a pivot that capture everything floating through the air. Traps were located at points up and down California’s Salinas Valley, and the rods were changed out every few days during the course of two seasons. By extracting the DNA from everything stuck on the rods, Choudhury could test for the presence of downy mildew spores using a highly sensitive, highly specific technique known as qPCR. This technique amplifies a segment of DNA unique to the species of downy mildew from spinach, Peronospora effusa. By monitoring the amount of amplification necessary to detect the specific DNA segment, a researcher can also determine the number of spores captured.

With volumes of data on hand, Choudhury applied epidemiological analyses to find patterns. He found that the number of captured spores showed an exponential increase over each season. Furthermore, within that overall trend there were regular pulses of spores that may have corresponded either to pathogen generation time or to spinach harvest cycles. Either way, ever-present spores are bad news for growers.

In another sleight of analysis, Choudhury estimated the dispersal distance of the spores from an outbreak. Of course the farther a spinach field is from an outbreak, the fewer spores will arrive at it. The question is how far the spores will travel. According to Choudhury’s models, there is some likelihood that there is a limit to the distance that the vast majority of spores will travel, but there is a higher likelihood that a significant proportion of spores will travel very long distances, potentially endangering spinach fields in remote locations in the valley. These data were rather noisy, though, and did not completely rule out the former scenario. On the ground, Choudhury showed that an active outbreak would lead to a higher level of infection 5.6 meters away, but beyond that the infection rate was no different from the background rate.

Dr. Choudhury also did a trial of mixed varieties of spinach. The reason for mixing varieties with resistance to different races of a pathogen is twofold. For strictly market reasons, if one pathogen race takes out a variety, the remaining resistant varieties will still produce. A grower never knows which races will be present, and so will have to grow multiple varieties to insure a harvest. However, the current practice is to grow the different varieties separately in wide strips because the growers worry about inconsistencies in leaf traits. This arrangement misses out on the epidemiological benefit of growing the mix of varieties in a single bed.

If a field is full of plants that are genetically identical, then a single infected plant will give off spores that are adapted to every plant in all directions. However, with a good mix of varieties, the plant’s neighbors may all be resistant to those spores, and any spores that land on resistant neighbors will be subtracted from the total pool of spores available to spread the disease. This dilution of susceptible hosts can slow the spread of disease. The intercepted spores may even pre-arm the neighboring plants against races of the pathogen that are adapted to them, a phenomenon known as induced resistance.

Dr. Choudhury showed the growers his mixed-variety field and challenged them to point out non-uniform plants; they could not. Unfortunately, the trial was disappointing. Although few varieties succumbed to downy mildew, resulting in a lower-than-expected total disease incidence for a mix, the disease incidence still crossed the 1-5% threshold. It may be that there have already arisen too many pathogen races for this method to succeed. The only scenario where mixed-variety plantings might work would be if the method were widely adopted across the valley.

The reason that new races continue to emerge is that growers depend too heavily on a small number of varieties that are resistant to the known races. With the vast acreage of the Salinas Valley planted to just a few varieties, the fast evolution of the pathogen will generate races that are pathogenic on these varieties as well. One strategy to put the brakes on this fast evolution would be to discard seed lots with too many sexual spores of the pathogen. This type of spore is where a new genotype can be formed, and with enough new genotypes, a new pathogenic race can arise. However, the seed producers, who are located in states to the north, might not be willing to discard a portion of their product for the benefit of the Salinas Valley system.

A couple of practices that Choudhury was not able to challenge were planting density and irrigation. The demand for organic lettuce has burgeoned, and now the standard practice is to grow a high-density lawn of spinach on 80-inch beds that stretch off into the horizon. Spinach production fills a huge area of the Salinas Valley, nicknamed the nation’s salad bowl. The endless expanse of spinach is a giant petri dish for pathogens, and the crowding insures a continuously humid layer that promotes spore germination. To make matters worse, the growers overhead-irrigate, absolutely insuring excellent spore germination conditions.

Big organic growers have been lured by the profit motive to shift to an industrial mode of spinach production without regard to agroecological realities. In so doing, they created a downy mildew crisis, and they have called in the plant pathologists to deal with the problem. It makes one wonder how much of what plant pathologists do is simply trying to clean up the disasters of industrial agriculture. Large-scale organic spinach is just as industrial as conventional agriculture. Resistant varieties, perfectly timed biofungicide application, disease scouting, and hand roguing might get this season’s crop to market, but without an agroecologically sound system design, these measures may not save organic spinach production into the future.

the Feds (should) Feed Families

“Feds Feed Families”. A key responsibility of the Federal Government is to assist those who struggle to make ends meet but occasionally come up short. That’s not what the Feds Feed Families campaign is about, though. No, it is campaign to encourage employees of the Federal Government to make individual contributions to food banks, with no dedicated expenditures of Federal funds beyond the tax deductions that are available to those employees who are fortunate enough to have bought a house and thus come out ahead if they itemize deductions.

It is well known that government employees are paid less than industry employees with comparable qualifications. The tradeoff is that government employees are supposed to enjoy more generous benefits and greater job security. Under the Obama Administration, Federal employees were subject to a freeze on cost-of-living adjustments so that Obama could pay for his extension of Bush’s tax cuts for the wealthy. When the freeze was lifted, the adjustment was modest — remember that this Administration expected Social Security recipients to make do with buying lower quality goods when prices rise. Now, under the Trump Administration, Federal employees are worried about job cuts, or if they keep their job, facing having to do more with less.

How unreasonable, then, to expect Federal employees to shoulder the responsibility of providing for less fortunate participants in the economy. In the wealthiest country in the world, which has seen steady economic growth for many years, John Boehner’s excuse that the Federal Government is broke is ridiculous. The money is out there, but the Government is committed to not using it.

To be fair, employees of the USDA have access to harvests that are not meant for sale, and these are included in the Feds Feed Families campaign, a praiseworthy effort to prevent food waste. Also, there is a procedure for employees with backyard gardens to donate their excess bounty to food banks, for which they are given a receipt for the cash equivalent of the weight of the produce donated, once again a tax break to those who can afford a house.

However, in a perverse twist to an already perversely named program, employees who want to make cash donations are discouraged from giving them directly to food banks. Charities often encourage donations of cash over goods because they can use the cash to leverage a higher value of goods than the donor could purchase with the amount of the donation. Instead of this, the employees are directed to make “virtual donations”, whereby they find a food retailer that is capitalized enough to offer online shopping, pay for some food, and direct that it be donated to a food bank. In this way, wealthy food retailers make a profit on employee donations. Given the pervasive wage-depression efforts of big food sector corporations, the donations will feed the forces that exacerbate food insecurity at the same time that they feed the food-insecure.

Individual charity will never fulfill all the needs of struggling families, especially when it becomes a vehicle for enriching the wealthy. The solution is economic equity. The Feds — meaning the Federal Government — should take responsibility for the well-being of the people.

collapse

Disregarding agroecological principles can lead to collapse. Florida citrus growers learned this lesson the hard way. Researchers in California are trying to prevent a rerun.

Huanglongbing, or HLB for short, is a disease of citrus that was originally recognized by farmers in southern China. It causes blotchy yellowing of leaves, sour deformed fruit, and — most devastating — premature fruit drop. The cause is apparently the bacterium Candidatus Liberibacter asiaticus (CLas), but as the incomplete italicization of the name indicates, this bacterial species cannot be grown in the lab, and therefore it has not been subjected to the steps necessary to confirm it as the pathogen. The CLas bacterium is transmitted to citrus leaves and stems by the Asian citrus psyllid, a tiny winged sucking insect similar to an aphid. The bacterium lives quite happily in the psyllid’s gut, but it can only be passed on to the insect’s offspring when they feed on an infected plant. This is where the citrus tree comes it.

The psyllid makes sure it injects some of its gut bacteria when it feeds on a leaf in order to provide its offspring with a meal of the beneficial bacteria they will need for survival, notably a species called Wolbachia. The CLas bacterium accompanies the Wolbachia, and in a fascinating case of bacterial genetics, can only survive in the presence of the Wolbachia. CLas at some point in its evolution was attacked by a virus that incorporated its own DNA into the bacterium’s DNA, and this internal virus is always poised to start replicating and burst out of the CLas cell, killing it. When scientists try to grow CLas in a Petri dish, this is what happens. However, in the environment where CLas normally grows, the virus is kept in check by a molecule that the Wolbachia produces. This psyllid-Wolbachia-CLas relationship has led researcher Georgios Vidalakis to call CLas a microbe of the Asian citrus psyllid, with citrus as just a transient host.

Once CLas is inside its transient plant host, it can spread only very locally within the plant, causing the leaves on just one branch tip to yellow. This gives a very patchy appearance of yellowing on a tree during the early stages of an epidemic. The only way that CLas can spread to the rest of the tree is when the psyllid juveniles grow up and fly to other locations on the tree, as well as other trees in the orchard. One unfortunate consequence for the localized distribution of the bacterium on the tree is that pre-symptomatic infections cannot be detected by monitoring programs that test tree sap unless the sap sample happens to come from a twig that is infected, and therefore there is usually widespread disease before the presence of CLas is confirmed.

The Florida citrus industry was slow to respond to the emerging threat of HLB disease. Where a comprehensive program for early eradication of the disease would have been an order of magnitude more costly than a program of strict quarantine to keep the disease out in the first place, once the disease becomes well established it is yet another order of magnitude more costly to try to manage it, in terms both of treatments and lost income. At this point Florida citrus production has fallen to the level of the 1940s. At least one commentator would like to blame the decline on venom from Anita Bryant, the 1950s-era singer who leveraged her fame to become both spokesperson for the Florida citrus industry and the leader of a nasty campaign to deny civil rights to gay people. Either way, there is a certain level of blame that the industry deserves.

What were the agroecological principles that were violated, allowing HLB’s destructive march across the state? Extensive monocropping allowed psyllids to move unimpeded from tree to tree, orchard to orchard, and county to county. A narrow genetic diversity insured that every citrus tree in the state is a susceptible host for CLas and a reservoir for additional infection. Basic sanitation was not adequately prioritized, with growers unwilling to destroy infected trees and orchards for the benefit of the greater landscape-level agroecosystem. Greater plant diversity might have supported populations of natural enemies against the psyllid, and plant diversity plus a healthy level of soil organic matter might have supported a microbial community with antagonistic capacity toward CLas. Only now are Florida growers looking for alternative crops, going as far as trials of the dry-climate crop pomegranate, an effort that was plagued with fungal wood canker diseases.

Of course the economic system played a role. Industrial production demands low diversity, high uniformity, concentrated resources, and substitution of capital intensive inputs over agroecological management. Growers will maximize individual benefit by retaining infected trees and harvesting sour deformed fruit for the juice market in order to recoup some of their investment. And in a perverse dynamic of the system, there are rich landowners who will retain unproductive trees on their property in order to classify their land as agricultural and qualify for government benefits. These growers are uninterested in the wellbeing of their trees or the industry as a whole, and from th perspective of industry itself they are wrecking any coordinated plan for eradicating the psyllid through spraying. With just one non-compliant grower, the psyllid finds refuge and can re-establish in the surrounding orchards, and thus the economics beats even conventional agriculture’s trump card.

The Asian citrus psyllid has already become established across a wide swath of California, but so far only a couple instances of HLB have been discovered in the Los Angeles area, out of ten thousand samples tested last year alone. The infected trees were destroyed, and movement of citrus material out of the zones of quarantine surrounding them is strictly prohibited, but unfortunately the psyllids will not be observing the quarantine boundaries. Researchers are scrambling to find resistant citrus germplasm for breeding resistant crop genotypes. New diagnostic tools are being developed for early detection that will register infection in sap samples from any part of an infected tree. Proponents of genetic engineering are scolding that their technology will have to be deployed to address conventional agriculture’s colossal wipeout on the technology treadmill it was already on.

One bright spot in the efforts to protect citrus in California is the work of the aforementioned Dr. Vidalakis. He is in charge of clearing all the citrus imports that are held in quarantine. Thanks to the foresight of policy makers in the 1930s, direct importation of citrus into the US is prohibited. Instead, all citrus material that someone wants to bring to the US passes through Vidalakis’ facility. From every sample of budwood his technicians painstakingly collect the microscopic growing tip, a piece of tissue out of reach of the plant’s sap and therefore of CLas or any sap-inhabiting viruses. They graft the tip onto a test plant, where it grows out and gets tested for all known viruses and bacterial pathogens, and also grafted to very susceptible plants that would presumably show symptoms in case of unknown viruses. Within a matter of months the importer receives certified virus- and CLas-free budwood, and citrus trees across the state are protected from devastating epidemics.

An admirable aspect of Vidalakis’ work is that he takes all comers. Immigrants from Asia can collect cuttings from their favorite citrus tree growing in their grandmother’s garden and submit them for high-tech cleanup. Vidalakis is not an agroecologist or social equity campaigner, but as a plant pathologist he recognizes that small-scale and backyard citrus growers are a legitimate component of the otherwise highly capitalized statewide citrus agroecosystem. If the small growers were marginalized, they would become the weak link in the protection of an entire industry.

Will the California citrus industry escape destruction from huanglongbing? It’s a cliffhanger. If industrial citrus production is able to overcome this agroecological reckoning, will it continue to present a sea of low diversity vegetation, a ready resource for the next intractable pest or pathogen from overseas or newly evolved domestically? Or will visionaries, a movement, and socioeconomic change arise and incorporate citrus production into a sustainable agricultural system designed using agroecological principles? There is never a bad time to turn to agroecology.

fungi go bananas

Plant pathologists have a sense of mission.  Take Ioannis Stergiopoulos.  Professor Stergiopoulos studies sigatoka disease of banana.  In case you are inclined to dismiss bananas as just a snack food, Stergiopoulos is ready point out that bananas are one of the top five staple crops in the world.  However, because they are clonally propagated, the world banana crop is dominated by a single variety and thus particularly vulnerable to potential emerging diseases.  Stergiopoulos also points out that pathogenic fungi in general are an emerging threat as they evolve new virulence genes.

 

Sigatoka is a complex of three diseases caused by closely related fungi.  Yellow sigatoka, caused by the fungus Pseudocercospora musae (P. musae for short), has been known for over a century.  Black sigatoka, caused by P. fijiensis, was discovered in 1963.  Eumusae leaf spot, caused by P. eumusae, was discovered the most recently, in the mid-1990s.  There is a progression of aggressiveness in the three species.  When black sigatoka arrives in a country that has only yellow sigatoka, it effectively displaces it, and then eumusae does the same with black sigatoka.  Black sigatoka can infect banana cultivars that are resistant to yellow sigatoka, and eumusae can infect cultivars resistant to sigatoka of either color (technically, to satisfy the plant pathologists, it is the pathogen that does the infecting, e.g. P. musae, and the disease is the result, e.g. yellow sigatoka; I will use “black sigatoka” as an abbreviation for “the black sigatoka pathogen”, etc.).  And while black sigatoka currently causes the biggest yield losses of the three, eumusae, which has not yet encircled the globe, is in a class with black sigatoka in terms of virulence.

 

Where do such diseases come from?  Stergiopoulos addresses that question using his extensive tool kit of genomic techniques, with which he can look at all the DNA that each species possesses and dig out trends in the genes.  His team analyzed mutations in 46 genes that are common to all species in the class of fungi that the three pathogens belong to, genes that seem to be important enough that they evolve very slowly.  This analysis showed that while the three belong to a single lineage, black sigatoka branched off first, while the other branch gave rise to yellow sigatoka and eumusae later.  They then looked at the family tree of these three plus other members of the class (remember that a class contains many orders and an order contains many families — maybe that would make it a class tree?) and overlaid the tree on the timeline from the first appearance of the class in geologic time in order to date the branches.  Black sigatoka branched off between 30 and 40 million years ago, while the other branch split into yellow sigatoka and eumusae lineages between 17 and 23 million years ago.  So not only does black sigatoka predate yellow, the reverse of their appearance in banana plantations, but all three predate the 20th century by more than a little.  So why the delay?

 

Of course there were probably other lineages that were branching off all this time — why should only these three species have become pathogenic?  Quite likely they were not pathogenic or else possessed little virulence when they first split off.  Pathogens have to acquire or adapt genes that let them take advantage of hosts.  Stergiopoulos’ analysis is able to give an idea of just how.

 

The three species’ genomes were found to contain a large proportion of transposable elements.  These are strings of DNA that contain genes that will copy the information in their own DNA string to another place in the genome.  This kind of random opportunistic jumping of segments of DNA to new sites tends to play havoc with the existing set of genes, but it can also occasionally cause advantageous outcomes.  The transposable elements can cause duplication of various genes, and sometimes the duplicate genes can evolve to take on new functions.

 

For a fungus to be a pathogen at all, it has to overcome a host plant’s defenses.  It does this with proteins called effectors, which disable components of the plant’s defense system.  A fungus can have the genes to produce a suite of different effectors, each one capable of taking on a different strategy that the plant can muster.  An expanded suite of effectors that can each evolve individually can be to the fungus’ advantage.  Stergiopoulos’ team found over 100 genes in each of the three sigatoka pathogens that show the genetic signature of effectors, and for each species about half of these genes arose after the lineages separated, quite possibly through evolution of duplicated effector genes.  Every time one of these effectors evolves to a point where it knocks out a host defense, the fungus gains an incremental advantage in growing and reproducing at the plant’s expense.

 

A pathogen also needs to be able to use the host’s resources for its own growth and reproduction.  A key aspect of this resource hijacking is the ability to digest the host’s cell walls.  The team found that black sigatoka and eumusae have had duplications of many of the same genes used for cell wall digestion, and this was a result of pure coincidence.  This parallel evolution is in some sense an adaptation to the host plant.  An increase in virulence afforded by enhanced cell wall digesting ability could also allow the fungi to grow and spread more easily, which we would then come to our attention as an emerging disease.

 

The team wanted to know what other genes might be different between yellow sigatoka on the one hand and the more virulent species on the other, in order to get a fuller picture of the traits that make a fungus more virulent.  They compared the three species’ genes to annotated lists of genes of known function in all eukaryotes (plants, animals, fungi, protozoans, etc.), paying special attention to genes that had gotten duplicated.  The result that popped out was an increase in copies in black sigatoka and eumusae of genes associated with metabolism — genes for transport and metabolism of amino acids, fats, carbohydrates, and secondary metabolites and genes for energy use.  Since the two species have achieved higher virulence, the team believes that an increase in pathways for metabolism is key for virulence.  One could imagine that when cell-wall-digesting enzymes liberate a plant cell’s juices, a fungus that has greater capacity for handling the spoils would insure that more of the goodies go toward its own growth and reproduction, rather than letting nearby opportunistic fungi take advantage of them.

 

Thus, the Stergiopoulos team has done a magnificent job of presenting the How of the evolution of virulence — gene duplications, evolution of effectors, increased ability to digest cell walls, and increased capacity to use the resources liberated.  What is outside of their purview is the Why.  Why should three species that have been evolving for millions of years all turn virulent in the 20th century?  Researchers who love mining genomes for scientific treasures will use plant pathogens as prospecting grounds, and they will justify their intellectual pursuits to funding agencies by promising insights into developing targeted disease control methods.  Meanwhile the environmental and economic factors that lead to the emergence of new pathogens are no secret to molecular plant pathologists, but they are just not as interesting to people attracted to the minutiae of genetic information.

 

And what are these factors?  Environmental factors include monocropping, sequential cropping of the same species, low genetic diversity, and movement of plant material across continents and oceans, all the product of human intervention.  Bananas are a special case, being sterile triploids that present problems for breeding, and being propagated from side shoots that can be planted across fields and countries leading to essentially one big banana plant with zero diversity divided up into multiple stalks across the landscape.  When a fungus can grow unimpeded over a vast area year after year, every cell division and every mating is an opportunity to evolve to better take advantage of a plentiful host.  When infected material is transported by long-distance travelers, a previously unknown disease from the Sigatoka District of Fiji can end up with a worldwide distribution.

 

However, many of the factors underlying the environmental are the economic.  Corporations seeking to make money selling a product find an agricultural commodity that is easy to produce, tolerates long-distance shipping, and presents a uniform quality that shoppers expect on supermarket shelves, they plant it in machine-harvestable rows at the maximum density, they fertilize it into a succulent treat for a fungus, and they promote it in extensive advertising campaigns that make an exotic tropical fruit seem like a necessary addition to a bowl of cereal in a country without a banana industry.  The profit motive overrides environmental and phytopathological considerations.

 

With this backdrop, the efforts of molecular plant pathologists can actually serve to consolidate corporate dominance of agriculture.  Moneyed interests recruit scientists to find high-investment technologies that will favor the biggest growers.  Plant pathologists deceive themselves into believing they are feeding the world, when they are actually propping up corporate profits, leaving the hungry still hungry.  Even the claim of saving a widely grown staple crop is equivocal, with a significant portion of the world harvest being industrially produced by multinational corporations for export.

 

We need scientists who are experts on plant diseases who can aid us in diagnosing our crops, advise us on designing our agroecosystems, assist our efforts in harnessing crop evolution, and warn us about emerging threats.  But when food becomes a commodity, scientific expertise becomes captured and misdirected.  What would an economic system look like where food is not a commodity?  It will take many minds to work out all the details, but it probably will not include a banana on your daily bowl.

myths about the obesity crisis

I finally got around to reading Julie Guthman’s 2011 book Weighing In: Obesity, Food Justice, and the Limits of Capitalism.  In it Professor Guthman pokes holes in many of the tenets of conventional wisdom regarding obesity – notions that obesity is mainly a function of calories in versus calories out, that the built environment causes obesity, that obesity is necessarily the cause of disease, that eating local organic food in season will reduce obesity, and others.  One particularly interesting current of scientific findings she presents is the role of pesticides, food additives, artificial sweetners, and environmental toxins in causing obesity, a connection that fits well with otherwise puzzling trends such as the sudden upturn in extreme obesity beginning in the 80s and the appearance of obesity in infants, as well as with the common knowledge that diets don’t work.  Of course, as the subtitle suggests, she connects all this with the role of capitalism in using human bodies as a fix to overcome its structural crisis (you’ll have to read the book to get the details on that one).

Most relevant to agriculture is her examination – or as social scientist Guthman would phrase it, “complication” – of the claim that crop subsidies create cheap junky food.  The original idea is that sugar and corn are cheap because of crop subsidies, creating the plethora of empty-calorie snack foods and soft drinks that attract unwary shoppers on a budget, while more wholesome foods are avoided as less affordable.  In reality it is modern food production methods that are at the root of food prices and availability.

For starters, the very nature of commodities like grain and sugar makes them cheaper than fresh fruits and vegetables.  Grain farming has become completely mechanized, with next to no labor used in harvest or horticultural practices, and the finished products can be handled similar to non-food commodities.  By contrast, most fresh fruits and vegetables are hand-harvested, there is often transplanting, pruning, thinning, and weeding involved, the products must be handled in a cold chain where they are kept refrigerated from field to supermarket, the ones that do not meet cosmetic standards are culled, and the short shelf life necessitates a fast track to retail.  Nevertheless, as with commodity crops, the modern price of fresh produce is down from the historic price, even without subsidies.  Food in general is cheaper.

What makes it cheaper?  It has to do in large part with the incentives of farmers.  As Guthman points out, farmers are price takers.  They have only their crops to sell to make their money, and most do not have a way to hold their crops back from the market waiting for a better deal.  Thus, distributors with the infrastructure to handle and store the products set the farm gate price.  Furthermore, consumer demand does not expand to absorb surpluses, in spite of price drops.

Farmers have sunken costs in land and already-planted crops.  Their only means to get a return is by producing more output as individuals, despite the drop in price caused by the sum of all producers cranking out surpluses.  For a farmer, any return is preferable to zero.  Thus, farmers seek investments, techniques, efficiency advances, cheaper labor, and new technologies to squeeze out that extra increment of yield per unit of input, and even increase their output further to make up for the fall in prices.  Government policies of increasing yield play right into this dynamic, from Agriculture Secretary Earl Butz’s 1970s dictum to farmers to plant fencerow-to-fencerow, to the everyday work of state and Federal research laboratories (such as the one where I have a job) that is conducted to increase farm productivity.

It is this ever-increasing production that has brought down food prices.  Cheap food is another goal of a government that is overseeing stagnating wages, most notably in the very food sector itself, but cheap food has had devastating consequences for farmers.  In the 1930s, crop subsidies were first introduced, not as a way to provide cheap food commodities, but as an aid to farmers to deal with food being too cheap.  While the reality of government payments has been problematic, with the funds often going to enrich wealthier farmers rather than to prevent destitution of farmers who are struggling, subsidies can be viewed as an effect of cheap food, not the cause.

As for the availability of junk food, manufacturers are always seeking ways to push against the limits of consumer demand.  Snack foods are engineered to contain maximum temptation and addictive quality, to bypass rational decisions regarding nutritional value.  The highest return on investment, and thus the greatest incentive for production, will come from foods that have the cheapest ingredients and most reliably trigger the eating response.  Thus, the widespread availability of junk food is a result of the capitalist system itself, not of government programs to mitigate the excesses of capitalism.

Guthman reserves some of her harshest criticism for the alternative food movement – health food, organic food, local food, artisanal food, even food justice.  I had noted problems with the organic food economy starting in grad school.  Word then was that organics would take off if they could just solve the price issue.  At the same time, the Soil Association was pointing out that we pay too little for food to make agriculture sustainable.  From my perspective living in a low-income neighborhood of marginal housing and hearing arguments such as as the downside of cracking down on older, highly polluting cars driven mostly by low-income drivers, I concluded that the solution was not to cheapen food, supply substandard housing, and weaken environmental standards, but rather to abolish low incomes, so to speak.  Later, when I heard about a plan to start a farmers market in Oakland to bring black farmers into town to sell to low-income black urban residents, I wondered how a community with few resources could support farmers trying to support themselves.  Not surprisingly the market failed.

Guthman articulates a more comprehensive analysis of my basic insights.  While the various currents of the alternative food movement started out as a pushback against problematic practices in the food industry, they ran up against the power of monied interests and re-channeled their efforts toward individual actions.  Instead of getting at the root of the problem, they have largely become lifestyle choices of the upper classes.  They allow wealthy consumers to opt out of the unhealthy aspects of the food system, to feel good while eating well – the dietary equivalent of NIMBYism – without challenging this system that condemns less-advantaged populations to poor health.

Weighing In serves as an important course correction to efforts by well-meaning activists who want to transform the food system.  Using our dollars to change a system that encourages individual options only plays into that very system.  It is worth our while to pay attention to social science researchers like Guthman.

ecologists on intercropping

Why isn’t there more intercropping?  It is common in the global south, but in the north, whereas cover cropping and rotation are mainstays of organic agriculture, intercropping is an exception.  Some authors cast doubt upon reports of overyielding, the term for an increase in total yield by a mix of crops grown together compared to the component crops grown in monoculture.  Ford Denison for one maintains that, in the intercropping studies he is aware of, the component monocrops are generally not grown at the appropriate density, and that the trials are not continued for enough seasons.  Beyond that, in mechanized agriculture the machinery is traditionally designed for monocrops, and besides a handful of crop combinations known to work well under particular circumstances, there is a shortage of research into what makes a productive intercrop.

In response, an international consortium of researchers led by Rob W. Brooker, in a 2015 New Phytologist paper that was one of the journal’s top ten most-cited papers of 2016, presents food for thought and promising directions for future research in intercropping.   These are ecologists, agronomists, and plant physiologists who look to recent advances in their fields that can be applied to intercrop design.

The basic premise of intercropping is that different species grown together can either benefit each other or escape the kind of competition that individuals of the same species would experience, through the differential use of resources known as niche complementarity, through actually helping each other by facilitation, or through more complex effects on the environment or other organisms.  The question is how to harness these effects.  One important point of Brooker et al. is that facilitative interactions between plant species predominate more in environments with greater stress, meaning conditions where environmental factors such as water, temperature, nutrients, or disturbance are significantly limiting upon plant growth, an ecological principle known as the Stress Gradient Hypothesis.  They suggest that differences in environmental stress might be responsible for variability in intercrop results.  Indeed, an advantage gained by mixed cropping in a poorer environment would be consistent with the more extensive practice of intercropping found among more marginalized farmers.

Some insight into potential avenues for improving intercropping comes from grassland ecology studies.  For instance, phylogenetic distance, meaning the degree of relatedness between species (or more precisely, unrelatedness), is a significant determinant of grassland productivity, with greater productivity found when more phylogenetically diverse grassland species are growing together.  Also, the association between diversity and greater productivity becomes more pronounced over time, an effect that is due to increases in soil organic matter and soil nitrogen, which lead to more optimum carbon and nitrogen cycling, what organic growers might call soil improvement.

Other insights come from plant physiology and plant-soil interactions.  Intercrops can show increased resource use efficiency, which is an increased production of biomass without any increase in a given input, such as light or water.  Deep-rooted plants can make use of different soil water stores than shallow-rooted plants, and can even redistribute water to their companions.  Some crops have adaptations for correcting soil pH or otherwise solubilizing minerals by exuding compounds into the soil, to the benefit of all plants in that soil.  Of course, legumes are known to interact with companion crops in terms of compensating for nitrogen removed by companion crops, and can even release nitrogen for their neighbors to take up in some circumstances.  Also, legumes shaded by companion crops generally make more efficient use of the reduced light.

In a bit more of a stretch, the field of microbial evolution finds that bacteria evolved in mixed-species communities are more productive than those evolved in monoculture.  Indeed, Brooker et al. remind us that modern plant breeding, an abbreviated type of evolution, has generally been carried out using monocultures, whereas the traits that allow a crop species to function well in an intercrop may be different from those that show an advantage in monocrop.

The consortium concludes by calling first for simply testing new combinations of crops that possess qualities already known to function in intercrops.  In regard to the machinery issue, an allusion they make to precision agriculture leaves it obvious that, with sufficient commitment, modern machinery can be designed to do anything.  Beyond that, breeding crops explicitly for use in intercrops would likely improve resource use efficiency, including selecting for traits deemed complementary and even using computer modelling of ecology research findings involving resource capture.  Meanwhile, considerations of phylogenetic distance and long-term coevolution are in need of more investigation before they can be applied to intercrop design.

Agriculture researchers, agricultural machinery engineers, and crop breeders, take note!

R. Ford Denison’s Darwinian Agriculture

I am a fan of Ford Denison.  It was his lab that reconciled the fact of the legume-rhizobium symbiosis with the evolutionary theory predicting that such a mutualistic relationship should fall apart because of cheaters.  When I saw he had a book out on agriculture I snapped it up.

Only Denison could have written Darwinian Agriculture.  As both an evolutionary biologist and a past director of UC Davis’ LTRAS, the Long-Term Research on Agricultural Systems project, he is well versed in the two fields and can evaluate agriculture trends using an analysis that is rare among agricultural scientists.  For instance, the Green Revolution was initiated by grain crop varieties that were higher yielding not mainly because they were more responsive to higher inputs, but rather because they were bred for cooperation over competition.

A plant, say, rice, growing in a field of other rice plants with different genotypes, will compete for sunlight by attempting to grow taller than its neighbors.  If the plant can capture more sunlight, it will be rewarded by having a larger share of the next generation made up of its own offspring, offspring that will carry the parent’s genes that made it competitive.  This competition for sunlight comes with a cost, however.  By expending so much of its resources on all that stem tissue, it has less left over for seed production than it would if it had no neighbors with which to compete.  Meanwhile, the neighbors are also growing taller in an attempt to improve their own reproductive success.

What if all the plants in the field had identical genes?  Competition would then be a zero-sum game, whereby the amount of extra seeds that a plant could produce by out-competing its neighbors would not increase the representation of its genes in the next generation at all, considering that the seeds they would supplant would have had those same genes.  This shared genetic fate allows for the possibility of cooperation.  If a breeder comes up with a variety that does not grow tall, and if it is grown in monoculture, it can give a higher yield than a related variety that expends valuable resources on extra stem production.

Of course growing a single variety in monoculture is problematic for other reasons.  A pest or pathogen that is able to overcome the genetic resistance contained in that variety will be able to overcome the entire field in short order.  Without a diversity of genotypes for natural selection to operate on, there can be no survival of the fittest among equals.  Also, a plant variety without a competitive drive will do poorly against weeds.  Thus, Green Revolution seeds are sold with a package of manufactured inputs to compensate.  There are other undesirable outcomes of Green Revolution technology as well, but the evolutionarily sound principle of selection for cooperation remains useful.

Perhaps the best example of selection for cooperation that Denison presents involves chicken breeding.  Chickens are evolved to be individually competitive as much as plants are, and they will peck at each other to the point of reduced overall egg output.  One investigator, however, had the idea of selecting not the best individual chickens for breeding, but rather the best groups.  Chickens were kept in pens of four individuals, and the ones allowed to breed were those with the greatest number of eggs per pen.  In six generations fighting was way down and egg production was up.  Through group selection chickens were bred to be cooperative.  The key was to measure the output of groups rather than individuals, a principle that could be applied to small plots of crops as well.

Denison also returns to the example of cooperation in the legume-rhizobium symbiosis.  Legumes produce nodules on their roots to host bacteria that can convert atmospheric nitrogen into nitrogen fertilizer.  The plant rewards the nodule-dwelling bacteria, collectively known as rhizobia, with food that it produces from photosynthesis.  It would seem like a beneficial relationship to both partners, but any bacteria that could harness the plant’s feeding system without going through the trouble of producing fertilizer would do even better.  These “cheater” rhizobia are common, and evolutionary theory predicts that they should have long ago displaced beneficial rhizobia unless the plant could somehow pick and choose among rhizobia strains.  Denison and his students showed that legume plants can indeed punish a poor-performing strain enclosed in a single nodule, causing that strain’s reproduction to suffer.  However, because of various considerations, detailed in Professor Denison’s explanation of the Hamilton r coefficient, the legume’s sanction system is only just good enough to get the fertilizer it needs for the current season, leaving plenty of poor performers in the population that is released back into the soil.  With this in mind, Denison comes up with a scheme for breeding legumes for stronger sanctions, involving the use of a test crop to evaluate the legacy rhizobial benefit left by the previous season’s plant, and then going back to breed from the seeds that had been collected from the plants that were subsequently shown to have left the most beneficial rhizobia behind.

Denison has an opinion on genetic engineering of crop plants that is different from most.  He is not opposed to genetic engineering in principle, but maintains that most such research will have little to show for the vast sums of money spent on it.  The reason is that the kinds of intervention that are possible by tweaking genes have already been tried over millions of years of evolution and thousands of years of coevolution, and any unequivocally beneficial simple modifications have already been adopted.  Additional modifications involve tradeoffs and are not likely to make a significant difference.  He does leave open the possibility of modifications that are too complex for evolution to have stumbled upon, such as re-engineering the chloroplast to recycle the byproducts of photorespiration, but most modifications of that level of complexity are beyond the scope of genetic engineering.

My biggest complaint about the book is the straw man that Denison sets up to provide a false balance for his critique of genetic engineering.  He selects some of the philosophers of alternative agriculture such as Wes Jackson and uses them to stand in for the science of agroecology.  He then provides a very reasoned scientific critique of some philosophical exhortations to farm using nature as a model to mimic, using his arguments to attack a certain conception labeled “agroecology” while ignoring the science of agroecology as actually practiced.  Agroecological scientists do indeed look to natural systems − as well as to traditional agriculture − for principles that can be used for improving modern agriculture, but then they test any ideas that come from such an examination.  That is what makes agroecology a science, and Denison even advocates for this kind of examination and testing.

Throughout the book I find many other points that I want to respond to, but on the whole the work is valuable, and a blog post cannot fully do it justice.  Denison is a very accessible writer, and part of the book is background on agriculture and on evolution for the uninitiated.  The text is peppered with interesting tidbits, such as the wasp that can smell when a butterfly is about to lay eggs and pursues her or hitches a ride on her to parasitize those eggs after she has left them.  Most importantly, though, agriculture cannot escape the principles of evolution, and Denison has provided plenty of food for thought.

biocontrol hits the dirt

Biocontrol agents targeting soilborne plant disease organisms have not lived up to expectations,‭ ‬according to a new review by Mark Mazzola and Shiri Freilich in the journal Phytopathology.‭  ‬Whereas classical biocontrol‭ ‬−‭ ‬the release of a pest‭’‬s natural enemy into an agricultural system to control that pest‭ ‬−‭ ‬has‭ a long string of ‬proven successes in the control of aboveground pests,‭ ‬there has been only limited success of species introductions into soil for controlling disease-causing organisms.  Typically a biocontrol agent introduced into soil will have a very low survival rate.

From an agroecological standpoint,‭ ‬the failure of introduced species to establish a presence in soil is not a surprise.‭  ‬Any two areas of soil can have multiple differences,‭ ‬including sand and clay content,‭ ‬mineral type,‭ ‬organic matter level and composition,‭ ‬vegetation history,‭ ‬water regime,‭ ‬microflora and‭ ‬-fauna,‭ ‬and even crop genotype,‭ ‬all of which can affect survival of a microbe.‭  ‬The existing microbial community is the one that makes the most sense for the particular set of conditions,‭ ‬and the conditions change over the seasons.‭  ‬As microbiologists like to say,‭ ‬everything is everywhere,‭ ‬and the environment selects.‭

This observation reminds me of the time when as a teenager I saw a play by Anton Chekhov.‭  ‬Everyone in the play was leading a troubled life,‭ ‬and no one seemed capable of breaking out of the‭ ‬established pattern and doing what would make them happy.‭  ‬I didn‭’‬t like the play,‭ ‬and I wished I could walk into the scene and tell everyone what they should do:‭  ‬“He loves you‭ ‬−‭ ‬stay with him.‭”‬  “He‭’‬s fragile‭ ‬−‭ ‬be more gentle with him.‭”‬  “Don‭’‬t try to be what you are not just to impress them.‭”‬  An alternate,‭ ‬more mature assessment‭ ‬is that if I‭ ‬somehow‭ ‬ended up in that setting with those characters,‭ ‬I would likely be caught up in the same malaise and change nothing.

So it is with those microbe additions.‭  ‬You introduce a promising strain of‭ ‬Pseudomonas into a soil system,‭ ‬one good at controlling disease in potting medium,‭ ‬and it gets lost in the crowd,‭ ‬unable to mount a takeover of the existing microbial community because it finds the physical conditions unaccommodating or gets overwhelmed by the other characters in the community.

Fortunately,‭ ‬Mazzola and Freilich present a proven alternative.‭  ‬If you change the environment using certain management options,‭ ‬you can select for a microbial community that is suppressive to disease.‭  ‬One example is anaerobic soil disinfestation,‭ ‬a radical alteration of the soil environment where‭ ‬the grower incorporates a carbon source like rice bran or alcohol into the soil,‭ ‬saturates it with water,‭ ‬and covers it with plastic.‭  ‬Anaerobic bacteria use up the oxygen and produce organic acids,‭ ‬killing pathogens.‭  ‬Another example is biofumigation,‭ ‬where mustard seed meal or other mustardy residues are incorporated into the soil,‭ ‬hitting the pathogens with‭ ‬a‭ ‬fatal‭ ‬wasabi-burn.‭  ‬Even after treatments are completed and the crops planted,‭ ‬there is‭ ‬a‭ ‬lasting effect of pathogen suppression, an outcome not found with chemical fumigation.

The reasons for the continuing benefit from these treatments are complex, as expected, and still being worked out.  There is evidence pointing to an advantage given to endemic microbes, and suggestions that some microbial groups that are associated with biological control make up an increased proportion of the surviving microflora.  There is evidence that the carbon source used for creating an anaerobic environment can make a difference in the microbial groups selected.

Beyond soil treatments, there can be other ecological interactions that contribute to soil disease suppression.  Root secretions from plants of certain genotypes can foster the proliferation of pathogen-suppressive bacteria populations.  Plant genotypes can interact in a complex fashion with soil management interventions.  Is it any wonder that a reductionist approach involving isolation of a microbial strain from a disease-suppressive soil, quantifying the antagonism that it possesses toward a select pathogen in the lab, and releasing it into a novel soil environment will fail in so many cases?  An agroecological approach, taking into account the multiplicity of factors that are operative in soil, is crucial for managing soil disease in a real world situation.

And the next time you see a‭ ‬Chekhov play,‭ ‬sit back and enjoy the way the characters struggle within the bounds of their milieu, and then reflect on what difference you can make in your own world.

cover crop rotation

Can you grow the same cover crop year after year?  Harvested crops get rotated to prevent soil buildup of pathogens toward any single crop species.  When it comes to cover crops, though, the standard for my area is a mix of bell beans and barley.  Variations on the theme exist, with oats, rye, or wheat being substitutable for the barley, and even peas or clover taking over the role of nitrogen fixation in place of the bell beans.  The trouble is, the grains are all members of the grass family, and the nitrogen fixers are all in the legume family.  If you grow a legume-grass cover crop every year, shouldn’t the soil build up diseases of legumes and grasses?  If cover crop rotation is necessary, what non-grass could function as a grass?  And does a nitrogen-fixing non-legume crop even exist?

Maria Finckh and her colleagues have a handle on the subject, in two chapters in the compendium Plant Diseases and Their Management in Organic Agriculture.  Yes, bell beans do get soilborne diseases.  Yes, they share diseases with other legumes.  One pathogen, Aphanomyces euteiches, the cause of pea root rot, has spores that can survive up to 14 years in soil and threatens pea production in France.  And yes, small grains share diseases − even weedy grasses can harbor some of these diseases.  Organic and sustainable farming are completely dependent on nitrogen fixation by legumes, even for manure production by livestock.  What is a grower to do?

Fortunately, Finckh and colleagues have suggestions for disease management in legumes and small grains.  For annual legumes, it is advisable to plant these in only three years out of a six-year rotation, counting both harvested and green manure species, and it is critical to never use the same species back-to-back as a green manure and a harvested crop.  Perennial legumes should be grown for a maximum of three years.  There are some pathogens that target dicots in general, so grass family crops are a good choice to follow a legume (or presumably non-grass monocots like garlic, asparagus, or others).

Regarding the sharing of pathogens, there are some with very broad host ranges, some that target only a single species, and just about every possibility in between.  Bell beans are subject to chocolate spot disease.  Their recommended rotation frequency is 4-6 years.  Clovers get clover scorch and clover rot, but white clover is generally resistant to these.  There are diseases that affect alfalfa but not its close relative black medic.  Soybean is susceptible to few diseases of the other legumes, and its recommended rotation time is the shortest, 0-3 years, while that of peas is the longest, 6-7 years.  The pea root rot pathogen can infect many legume species, as well as beets, but it is peas that sustain the greatest damage.

One legume has me intrigued − serradella, Ornithopus sativus.  I had never heard of this, but based on the legume-disease matrix presented in the chapter, this species gets none of the common legume diseases.  It is less cold-hardy than some legumes, but evidently it is well suited to a maritime Mediterranean climate, as there is a feral population reported in Santa Cruz County.  However, it seems that the seeds are commercially available only from Australia or South Africa.

Regarding small grains, the advice is less involved.  Rye and barley can harbor the pathogen that causes take-all of wheat, so wheat should never follow rye or barley.  Oats, however, are resistant, and they may be suppressive to diseases.  Non-grass, non-legume cover crops include mustard-family crops, Phacelia tanacetifolium , and flax.  I have been trying out Phacelia, a member of the water-leaf family, as a green manure, and it is giving me good stand coverage where it has established.

Planning out a cover crop rotation is an important component of disease management, but it is best complemented by disease monitoring and identification, which will give a clearer indication of what crops can follow.  Beyond rotation, there are cultural recommendations for disease management.  Because many pathogens are persistent in crop residues, one should insure effective residue breakdown.  A healthy soil microbiome fed by plentiful organic matter from a variety of sources and crop types can be antagonistic to soilborne pathogens.  Wet or waterlogged conditions will promote certain diseases.  Some pathogens are seedborne, and thus a sanitary source of seeds is important.  For some diseases, particularly mildews, mowing is helpful, and even in the case of clover rot a late fall mowing may save some of the crop.  Planting mixtures can reduce disease.  And the dreaded pea root rot?  If you have a history of this and are thinking of planting peas again, the soil should first be bio-tested.

Bart Thomma on Verticillium

Bart Thomma gave an interesting talk on‭ ‬Verticillium dahliae,‭ ‬the pathogen that causes verticillium wilt, able to attack most broadleaf plants.‭  ‬The strains that are pathogenic owe their virulence to the gene with the code name‭ ‬Ave1.‭  ‬This is the gene that turns the plant‭’‬s defense system off.‭  ‬The interesting part is where‭ ‬the pathogen got that gene.

Thanks to advances in DNA sequencing technology, there are genome sequences of hundreds of species searchable on the web.  Genes that are very closely related to Ave1 are also found in a few unrelated fungal pathogens and a bacteria, but they are found most widely in plants, where they regulate water relations by controlling the opening of leaf stomates.  This evidence suggests that Verticillium dahliae (V. dahliae for short) picked up a copy of the gene from a plant it was living in and incorporated it into its own DNA.

How unusual, Thomma thought, that the pathogen should overcome the plant’s defense response by stressing it through dessication.  The gene product definitely had the machinery for controlling stomates.  The trouble was, when the Thomma lab modified the fungus, substituting stomate-opening genes from other species for the Ave1 gene, the fungus could no longer cause disease in the plant.  Stomate control was not the mechanism by which the fungus defeats the plant.

This led Thomma to approach the issue the hard way, adding the Ave1 gene product to a solution of plant cell components to see what it interacted with.  With the use of specially tailored antibodies, the interacting plant proteins can be pulled out of solution and then characterized.  This approach is hit-or-miss, but in this case there was a promising hit — plant chitinase.

Fungi have cell walls made of a tough substance known as chitin.  This is the same chitin that makes up insect and crab exoskeletons, but it evolved independently in fungi.  Chitinase, as signified by the “-ase” ending, is an enzyme that dissolves chitin, giving plants an important defense against fungi.  With further investigation, the Thomma lab found that the Ave1 gene product indeed has a powerful capacity to inhibit chitinase.

My jaw dropped.  The fungus got hold of a plant’s stomate-regulation gene, and it evolved a chitinase-inhibiting function.  That would be like buying a used windowsill air conditioning unit, tinkering with it to make it function as a dashboard radar detector, and yet still keeping its cooling capacity!  The gene ended up in the rapid-evolution portion of the fungal genome, the 3-12% of the genome where the fungus allows mutations to happen without constraint, where once in a great while evolution’s workshop comes up with an innovative weapon that disables the plant’s arsenal.  The lucky fungal strain uses such a newfound advantage to proliferate in the environment, and a new plant disease is born.