what’s wrong with my plants?

A year and a half ago I moved into a place with a yard. The yard had been neglected, and I was determined to beautify it. I planted both seeds and potted plants, and I can’t help noticing that there’s something wrong.

For one thing, the majority of the potted perennials died. They were purchased locally and consisted of plants adapted to the xeric conditions here. The annual wildflower seed mix did better, and had the curious property that different species bloomed in the different areas of the yard, even though all the areas received the same mix. Most notably, the wildflower patches in the back became dominated by the decorative flax, with two lupine species also doing well, but the other plants were stunted. The grass seed I sowed in the bare spots in the back lawn came up like tiny threads that never filled in the spots, but the perennial clover seed has grown aggressively. I love a good mystery!

Here are some of the clues: The houses in the neighborhood were built when modernist architecture seemed appropriate for living in — the 50s and 60s. Before that it was farmland. The soil is a swelling clay that shifts the foundation and distorts the door frames when it’s dry. The back lawn had suffered from drought when I got here, with only clumps of the hardiest grass surviving, although the lawnmowing service continued biweekly. The other parts of the backyard were covered by bark on top of weed cloth, with three stonefruit trees and a rosemary bush growing in openings in the cloth; I pulled up patches of the bark and cloth for the new plants.

I admit guilt in the death of one shade-loving perennial. I planted it under the the big tree in front, only to watch the the tree drop its leaves and the winter sun slip its rays under the branches to cook the poor plant. Another perennial turned out to be frost sensitive. Four other ill-fated perennials, however, seemed to do well until the summer, when they showed some wilting in the heat. I watered them, and they further wilted and died.

When I saw how well the lupines – native legumes – grew in the back, I planted two legumes from the faraway prairie – an annual and a perennial. The annual was stunted, and the perennial did not survive past seedling stage. Also showing stunting was the existing peach tree in the middle. One of the lupine plants collapsed suddenly while flowering. And now in the second season I see that one of the patches in back has taller and greener flax on the edges, while in the middle the flax is shorter and yellower.

What could be the matter? My first thought was nitrogen deficiency. Years of farming may have left the soil degraded, and biweekly removal of the grass clippings would have robbed the lawn of the nutrients the grass had been able to scrounge up. Clover and lupine do well under nitrogen-limited conditions because they harbor nitrogen-fixing bacteria in their roots. If nitrogen were plentiful in the soil, the grass would be expected to out-compete the clover, but a pioneering study by Stern & Donald working in Australia in the early 1960s showed that clover will win the competition if nitrogen is low, thanks to that self-fertilizing capability. The back lawn seemed like a clear example of this second scenario.

What about the other stunted plants? Could they also be suffering from nitrogen deficiency? Shouldn’t the prairie legumes have done better with their own supply of nitrogen fertilizer? Maybe not. These two species host different strains of nitrogen-fixing bacteria from those of clover or lupine. The clover seeds came coated with their preferred strain. The lupines, growing in their native range, might have found suitable strains already present in the soil. Perhaps the prairie legumes, far out of their range, found no bacteria they could work with and ended up starved for nitrogen.

Nitrogen deficiency might also explain the shorter yellower flax plants in the center of the one patch. The plants on the edge presumably have access to soil outside the patch where no competing plants are growing. It is conceivable that a dose of extra nitrogen from the outside would give these edge plants a darker green color and an extra increment of height.

So is the nitrogen limitation hypothesis correct? What about some of the other observed phenomena, like the vigor of the flax, the collapsing lupine, or the lack of history of mowing in the formerly mulch-covered seedbeds? Considering the lupines again, these are unusual among legumes in that they do not form mycorrhizae, the mutually beneficial relationship in which specialized fungi grow within a root and extend out into the soil, helping the plant take up phosphate and other minerals in exchange for sugar from the plant. Non-mycorrhizal plants have roots that use other tricks to maximize phosphate uptake. Is there a way that this peculiarity could be involved in the differential growth?

As a first approximation, the mycorrhizal symbiosis is win-win arrangement, but deeper investigation has shown that different fungal strains vary in the amount of benefit that they provide the plant. Some cheater strains take the sugar and provide no benefits at all. Fungal strains that produce lots of spores are thought to be expending energy on these survival structures at the plant’s expense. Ecologist Jim Bever presented findings that a plant can tell if a root has been taken over by a cheater strain and can respond by shutting off the sugar spigot. This defense fails, though, when there is a mix of strains on a root and the plant can’t distinguish the cheater. The specialized fungi, for their part, have to be connected to a plant root to live.

The history of farming on this soil might have left a predominance of cheater strains. Farm fields often remain fallow at the end of harvest, leaving no crop roots and not even many weed roots to allow for the continuity of living mycorrhizal fungi. Instead, spores from more selfish strains are left to sprout when the next crop is planted. The mixing of the soil from tillage would have left the plants confused as to which were the cheater strains. Additional years of weed cloth cover might also have been particularly hostile to all but the spores from the selfish strains, with only the occasional stonefruit root supporting its isolated bloom of living mycorrhizal fungi. In such a situation the non-mycorrhizal lupine, carrying no burden of cheater strains, might be expected to have an advantage over mycorrhizal plants. Are there other non-mycorrhizal plants that might provide supporting evidence for the hypothesis of deleterious or absent mycorrhizal fungi? As a matter of fact, a closer look at the flax-dominated patches reveals a second layer made up of flowering sweet alyssum, a plant in the famously non-mycorrhizal mustard family. The other plant species in the mix are expected to be mycorrhizal, and these are stunted.

Except the flax. Does the flax disprove the hypothesis about absent or cheater mycorrhizal fungi? Not necessarily. Ecologist Nancy Collins Johnson showed that spores of mycorrhizal fungi found in soil after a soybean crop were parasitic on soybeans but beneficial on corn. And the grande dame of mycorrhizae research Sally Smith pointed out that some plants will form mycorrhizae without showing a growth difference. The flax might just have a different response to the mycorrhizal fungi in the soil from the other mycorrhizal plants.

While I’m exploring alternative hypotheses, I should consider the obvious. After years without plants, the covered patches would have lost organic matter. The soil foodweb would have unraveled, losing decomposing organisms ranging from microbes to earthworms. The soil would have compacted. Roots would have a harder time penetrating, and they would be short of the oxygen necessary to do their work. The plants might very well show stunting in compacted soil. Might the flax, the lupines, and the sweet alyssum just be better at dealing with compaction than the other plants?

Another possible cause of growth abnormalities is allelopathy, the inhibition of plant growth by plant-derived chemical compounds. The stunted peach tree happens to be right next to the rosemary bush. There are documented cases of aromatic plants inhibiting the growth of other plants around them through the chemicals they exude, such as the work of ecologist C.H. Muller on chaparral plants. My husband once got a splitting headache from breathing in the fumes of a rosemary plant he was chopping out – I wonder if anyone has tested the effect of rosemary fumes on the growth of peach trees. Another source of allelopathy could be the bark mulch. Decaying organic matter can release compounds that inhibit plant growth, and some of the better known of these compounds are breakdown products of lignin and hemicellulose, such as would be found in bark. Growing plants exposed to these cell wall components have their tissues prematurely hardened, often leading to a visibly pinched stem. Indeed, I saw a pinched stem on a second-season lupine growing from a seed that had fallen into the bark mulch. It was growing in the shade, and it collapsed as the changing sun angle in spring exposed it to more drying conditions. Might those compounds also have leached through the weed cloth and remained in the patches of soil, causing stunting of some of the other plants? Several of the species that failed to thrive in the formerly mulched areas bloomed beautifully in the other areas.

And then there are nematodes. The conventional wisdom for diagnosing a plant-parasitic nematode infestation, at least among non-nematologists, is that if a patch of plants fails to thrive, and if other factors such as nutrient deficiency or disease can be ruled out, suspect nematodes. These thread-like microscopic worms can damage roots and cause yellowing or stunting of plants. Whereas wildland soil also contains predatory nematodes that hunt down the plant-parasitic nematodes, agricultural chemicals will kill off the predatory nematodes, according to nematology professor Howard Ferris, leaving intact the populations of plant-parasitic nematodes. Interestingly, there was a study by Widmer and Abawi out of Cornell University that found green manure of two types of flax to be suppressive of nematodes due to the production of cyanide from chemical reactions in the chopped leaves. If the roots of the decorative flax could produce cyanide to deter nematode attack, then nematodes might be a neat explanation for the stunting of the other species.

None of these hypotheses are good explanations for the wilt-water-die pattern of the transplanted perennials, though. This pattern is a known phenomenon among some plants adapted to dry summers, such as members of the Protea family. Such plants may be champions of reaching and conserving water, but they are lacking in defenses against Phytophthora, part of the group of organisms known as water molds. As the common name suggests, pathogenic Phytophthora species take to water like a fish, producing spores that swim through saturated soil toward roots they sniff out. The pathogen that germinates from these spores rots the root it infects, interfering with water uptake. The amount of infection, coupled with warming temperatures, can reach a point where the plant wilts. The pathogen is favored by excess water, warmer temperatures, and neutral or alkaline pH. If you give a plant suffering from a Phytophthora infection lots of water when it wilts, the swimming spores will worsen the infection. Did I do that to those dry-adapted perennials?

There are other notable wilt pathogens. I once watched a pumpkin plant collapse over the course of an afternoon of gardening. A plant pathologist told me that it was probably Fusarium, a type of fungus that is the bane of organic farmers due to its ability to thrive in fertile soil high in organic matter. Some other wilt pathogens are Verticillium, Pythium, Armillaria, and Rhizoctonia, which are, respectively, a Fusarium relative, a water mold, a mushroom, and a mushroom relative.

The suspect lineup now includes wilt pathogens, plant-parasitic nematodes, allelopathy, compaction, cheater mycorrhizal fungi, and nitrogen deficiency. How would one single out the true culprit? An examination of roots would reveal whether pathogens were causing rot or nematodes were leaving lesions or cysts. In the case of the legumes it would also show the extent of nodules of nitrogen-fixing bacteria. Nitrogen deficiency in the soil could be revealed by a soil test. Compaction is measured using a penetrometer, but establishing the effect of the level of compaction on the growth of plants would take an actual experiment growing those particular plants in the compacted soil versus in a soil exactly like it minus the compaction. Allelopathy is tested by collecting the compounds using foam or resins that absorb them and then growing the plants in the presence or absence of the extracted compounds. Testing for cheater mycorrhizal fungi would involve isolating the strains of fungi out of the roots, a tricky endeavor given the inability of these fungi to live without a connection to a plant root, but doable. The plants would then be grown with or without the isolated strains to see if there is a growth difference.

And after all that work, it might turn out that several or all of the culprits had ganged up on the plants. Fortunately the solutions to all these problems are found in agroecology or ecology. Since the legumes are producing their own nitrogen fertilizer, they are increasing the amount of nitrogen in the yard. Recycling of lawn cuttings and other materials will counter the loss of nitrogen and nutrients, either through using them as mulch or in compost. Simply growing plants will eventually ease compaction, and if a diversity of living host plants is always available, any beneficial mycorrhizal fungi present will get a boost over spore-formers. Avoiding soil disturbance will also advantage the beneficial fungi. Growing resistant plants is one of the best strategies for dealing with nematodes and soilborne diseases. Planting a diversity of plants will help insure the presence of some resistant types, and the mechanism of environmental filtering will eliminate the susceptible ones. If any predators of nematodes are present, they will be conserved by avoiding the use of agrochemicals. There is even some research being done on organisms that eat soilborne pathogens, such as the recent paper by Pei Zhang and colleagues working out of North Carolina State, who found that a fungus-eating species of nematode and a fungus-eating species of springtail were able to reduce the loss of tomato seedlings to a common species of Pythium in a laboratory setting. Such fungus eaters can be encouraged to multiply in soil by organic matter addition (I know, Pythium is a water mold, not a fungus, but don’t tell the fungus eaters). As for allelopathy, I recall that there is a protective effect of greater plant biomass, such as larger seeds and higher plant densities, which seems to dilute the inhibitory compounds.

Did I miss anything? Would you do something different? Let me know your thoughts in the comment section. Now if you’ll excuse me, I have some yardwork to take care of.

it has already been decided

Plant pathologists are in agreement – GMO crops are safe and effective for controlling crop diseases and boosting yields. The only question is, why can’t they get their message through to the general public?

Peter van Esse works on Asian soybean rust, which is a destructive soybean disease in Brazil that is held at bay by extensive application of fungicides. The fungicide use could be reduced through breeding of resistant varieties of soybean, but there is no source of natural resistance in any known strain of soybean to breed into a crop variety. There is, however, resistance in some strains of pigeon pea, a relative of soybean, and the genes responsible for pigeon pea resistance have been thoroughly studied. Unfortunately, pigeon pea is not closely related enough to interbreed with soybean.

The technology exists for inserting the pigeon pea resistance genes into soybean. Van Esse has accomplished the transformation, and the tests show that the resulting transgenic soybeans can fight off the disease. The only obstacle is public opposition.

A colleague of van Esse’s points to an article on the topic in a social science journal – the people who know the least about GMOs are the most adamantly opposed to them. Why, they puzzle, is the public so poorly educated on the safety and benefits of GMOs?

Perhaps the question should be, is it any wonder? Science has a track record of making authoritative pronouncements, only to reverse them upon further study. Only N95 masks work against coronavirus. No, cloth masks work and are a necessity. No, cloth masks are useless. The coronavirus can’t be transmitted more than six feet, but it can infect you if it’s on a surface. No, it is airborne and can be carried more than six feet, and the dangers of contacting it from a surface are negligible. Coffee is bad for you. No, coffee is good for you.

It should be noted that science is a process. Teams of scientists work full-time to elucidate every factoid, every insight, every detail about the natural world. The truth is out there, but it takes time to piece together the full story. Like early election returns, early pronouncements may turn out to be wrong. And scientists make mistakes. The process of science includes mechanisms for catching mistakes, but sometimes mistakes can slip through

When science meets money, though, these mechanisms can really break down. Take the example of partially hydrogenated oils. In the early 20th century, chemists reacted hydrogen with vegetable oils to make fats that stayed solid at room temperature. These fats had a longer shelf life and were cheaper to produce than lard, characteristics that promised higher profits to the food industry. Partially hydrogenated fats were sold to the public as healthy alternatives to animal fats and tropical oils because they were engineered to be slightly less saturated and had no cholesterol. This industrial product became a staple of the kitchen, synonymous with shortening, and the base ingredient of margarine.

Some eighty years later word got out that the story was not so simple. As every beginning chemistry student is taught, chemical reactions proceed both ways. The ingredients come together to form products, but the products also come back together to regenerate the initial ingredients, with the strength of each process determining the equilibrium level of ingredients and products. However, while the hydrogenation reaction will regenerate hydrogen in its reverse mode, a molecule as complex as a polyunsaturated fat will not necessarily return to its original form. The original molecule is in the cis form, characterized by a kink in a long-chain molecule, but the regenerated molecule tends to be in the straightened trans form, even though it will have the same atoms connected in the same order. Unless the hydrogenation process is pushed beyond partial to complete, there will always be molecules created in the trans form.

So-called trans fats are found in nature, but they are associated with bacteria. In the human body, industrial trans fats elicit an inflammation response. When they enter the bloodstream, the inflammation is manifested in the arteries, and the result is coronary disease. The engineered product that had been assumed for generations to be just another form of fat turned out to be deadly. Decades of studies linking saturated fat to heart disease had to be discounted because the effect of natural saturated fat could not be disentangled from the effect of trans fat.

While trans fat has no connection to trans genes, the example is instructive. The FDA has declared that all transgenic crops are no different from ordinary crops and thus do not require special regulation. Could they have unforeseen consequences? The answer is not known, because you can’t discover what you don’t test for. And while proponents of transgenic crops take pains to point out the absence of harmful effects in the billions of animals that have eaten transgenic feed, the process of insertion of genes is not vindicated by the lack of harm caused in one instance. It would be like a teenager driving at 100 miles an hour down a stretch of road and concluding afterward that because nothing bad happened, therefore nothing bad happens from driving 100 miles an hour. Maybe other transgenic crops will be thoroughly tested for safety, but the unsettling lapses in reasoning stand out.

Soybean disease researcher van Esse goes on to describe the Dunning-Kruger principle, the observation that the people who are least informed on a topic overrate their ability to act regarding it. The irony is that van Esse himself confesses knowing nothing about the social situation in Brazil but nevertheless feels confident to act there to solve what he identifies as a problem. Brazil is the home of some serious problems, prominent among them being the shocking rate of biodiversity loss, which is accompanied by displacement of indigenous peoples, along with a gap between the haves and the have-nots that is one of the worst in the world. Unfortunately, soy is not a neutral player, but rather a major contributor to these three problems.

Thanks to advances in agronomy, the Brazilian dictatorship in the 1970s was able to initiate colonization of the previously inhospitable center-west of the country by large-scale soy plantations. Auspicious market conditions pulled in a flood of foreign investment, promoting explosive growth of the soy industry, and also solidifying control of key infrastructure by multinational corporations. The most biodiverse savanna in the world quickly lost ground to soy monoculture.

The government has considered soy to be a boon to the Brazilian economy. It has certainly been a boon to the multinationals. However, the expansion of the soy frontier has dispossessed smallholders in its path, leading to a crisis of landlessness among the rural population. Because of the high level of mechanization in soy, rural workers were left with scant opportunities. Indigenous peoples find their lands under assault by the encroachment of agribusiness, among other threats.

Demand for soy has only accelerated since then. Governments of the left and right promote the industry. The soy frontier is penetrating the Amazon. Multiple crops per year are grown in the tropical zones that once supported savanna and rainforest. The turnaround time got so short that the combine drivers harvesting the soy could literally see the planters in their rearview mirror.

In 2001 Nature stepped in to spoil the party, in the form of Asian soybean rust. As any plant pathologist could have told the growers, continuous monocropping provides a breeding ground for diseases. Overuse of fungicides leads to pathogen resistance. The Brazilian government was forced to impose an annual soybean-free period, a sort of social distancing for soy plants, in order to help the fungicides to bend the curve of soybean rust disease downward. However, instead of getting the message that environmental destruction and social dislocation must stop and that soybean production must scale back, Dr. van Esse and the growers saw the challenge to genetically engineer a resistant soybean.

Not all opposition to genetic engineering in agriculture is based on gut feelings and a skepticism of science. There are scholars of the larger socio-economic context of agriculture who have valid critiques of genetic engineering that are based on a more comprehensive analysis. Take recombinant bovine growth hormone, rBST. The underlying problem of the US dairy industry is overproduction. The action that individual producers rationally take to increase their income is to produce more, but the overall effect of the sum of these individual decision is to depress prices, and individual growers then struggle to break even. If the market were the only force determining production levels, producers would go out of business en masse, and the supply of dairy products would show boom-and-bust cycles. Government must step in with price supports to insure an uninterrupted supply, as well as a living for the producers.

Enter rBST. The gene for bovine growth hormone is inserted into microbial cells, which are grown up in a vat. The resultant hormone is purified and packaged for injection into milk cows, causing them to increase their milk production. No transgenic organisms make it to the cows receiving the injection, and no trace of the transgene can ever get into the milk. The FDA has determined that there is no difference between the milk from cows receiving rBST versus those not receiving it, and they may very well be right. Nevertheless, many dairy companies tout their products as rBST-free. So what’s the issue?

Some animal welfare advocates express concern that the conversion of a cow’s body into a souped-up milk factory through the use of rBST could be detrimental to other areas of the cow’s well-being. From a whole-system perspective, increased production is the opposite of a solution in a saturated market. Nevertheless, students of plant pathology express amazement that anyone would be opposed to dairy products that have the FDA stamp of approval. Plant pathology professor Pam Ronald, whose lab takes credit for breeding a flood-tolerance gene from a farmer-developed rice variety into high-yielding rice by using modern genetic analysis tools, regularly skirts whole-system issues in her vociferous promotion of transgenic crops.

Which is not to say that transgenic crop researchers are maleficent. They truly believe that their technology can be used to help the poor. Unfortunately, if you have a hammer, everything looks like a nail. They see the statistics of blindness caused by vitamin A deficiency in the developing world, and they want to help in their own special way. While they delight in creating green-glowing bunnies – these really exist – the poster child for genetic engineering is golden rice.

Vitamin A, in the form of beta-carotene, is found in every green leaf on the planet, and can be highly concentrated in many orange-fleshed plant organs. If you eat your vegetables, you can’t help but get your vitamin A. Are all those children in the developing world getting away with not eating their vegetables? The late Professor George Wolf, a vitamin A expert at MIT, used to point out that a mother can crush leaves and feed them to her child to provide vitamin A. If vitamin A is so plentiful in the environment, how can deficiency be so widespread? Perhaps the example of the modernization of Indonesian agriculture is instructive.

Traditional Indonesian agriculture consisted of small rice paddies surrounded by earthen banks upon which vegetables were planted. The Green Revolution, a previous generation’s program for increasing crop production without considering the context (which was machinations by the powerful to marginalize small growers, not lack of productivity), created high-yielding rice to replace the traditional varieties. The Indonesian dictator overcame technology skepticism by torching the fields of peasants who refused to convert their small paddies to extensive monocrops of Green Revolution rice. The banks of vegetables were gone, and the era of easy access to vegetables was over. While other countries have other stories, there is a general trend that Western modernization by top-down development schemes focusing on getting calories into the poor has caused the demise of vegetable cuisine in the developing world.

Besides vitamin A, vegetables are the source of many other important factors, such as folic acid, potassium, fiber, anti-oxidants, anti-cancer compounds, and more. Transgenic crop researchers saw the vitamin A deficiency, figured out how to make rice plants accumulate beta-carotene in the starch of the grains, and began a campaign to get golden rice into the mouths of poor children. Never mind that a high-carb diet with an accompanying dose of vitamin A will still leave the poor vulnerable to the kind of inflammatory diseases that plague the West. If you declare your opposition to golden rice, you open yourself to accusations that you don’t care about the poor.

The persecution gets worse. When a group of dissident UC Berkeley scientists discussed opposing the showing of a film promoting GMO agriculture on campus, they were subjected to a smear campaign. A middle school school teacher in Maryland who is also an oddly well-connected pro-GMO crusader summoned their email chain through a Freedom of Information Act request. He then spread false accusations of conflicts of interest against them around the internet, a charge that would be more appropriate against researchers receiving funding from large corporations. Ever wonder why I blog incognito?

Agricultural research grants usually require a public outreach component. Soybean rust researcher Van Esse wonders why plant pathologists haven’t done a better job convincing the public of the correctness of their solutions. Rather than better commercials, what the grants should require is consultation with activist groups, with the opinions of dissident researchers actively sought out. Ideally, considerations of profit should be excluded from discussions of the benefits and drawbacks of a GMO project. GMO researchers should approach outreach with the realization that they are not the most informed authorities about agricultural issues and thus are not as qualified to act as they imagine they are. And regulatory agencies should apply the precautionary principle, assuming that new technologies are risky until proven safe, rather than giving the green light and finding out in retrospect that a technology is harmful.

And when you hear money talk, take a listen to your gut. Then seek out the rest of the story.

Your turn

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smaller fleas

It was during smalltalk over a shared breakfast table on Amtrak that the man across from me began excoriating powdery mildew. He was a Colorado pot grower. His greenhouse operation held hundreds of plants, and the air circulating between his and the adjoining pot greenhouses was spreading the spores of the leaf parasitic fungus that had somehow gained a foothold inside. The greenhouse conditions provided an ideal environment for germination and growth of powdery mildew, and the high density of plants insured an endless supply of favorable landing spots for the dust-like particles that can each start a new colony. Despite the lore, pot plants are not indestructible, but rather serve as hosts to many pests and diseases, with powdery mildew being a leading factor threatening pot growers’ investment. Powdery mildew doesn’t kill a plant outright, but it weakens the plant and lowers the harvest quality.

There are about a hundred species of powdery mildew that make up this family of fungi. A powdery mildew’s thread-like growths cover the surface of a leaf and send root-like structures into the cells to feed. Its upright chains of spores give the impression of powder on the leaf. Powdery mildew is known as an “obligate biotroph”, meaning it can only survive on living host tissue. A key requirement of this infection type is that the fungus must come pre-programmed to neither kill the parasitized plant cell nor awaken the cell’s defense mechanisms, a balancing act accomplished through a tightly choreographed sequence of interactions with the cell’s machinery.

A reality of the plant world, though, is that distantly related plant species have distinct cellular machinery, meaning that a powdery mildew species that is not correctly pre-programmed, that is to say, coevolved with the plant it arrives on, will trip up and not be able to infect. Thus the powdery mildew on the sowthistle next door will not spread to your pumpkins, and the powdery mildew that emerges on the rosebush at the end of the row of grapevines and signals the grower to spray sulfur on the vines is not the species that actually infects the vines.

What the powdery mildew species have in common is similar germination requirements. The reason for this is that the spores carry their own moisture, allowing them to germinate without the liquid water that most fungal spores require. In fact, liquid water inhibits powdery mildew spore germination and can even cause the spores to burst. The spores do need a certain amount of humidity to germinate, but it can be as low as 50% relative humidity, and germination works better within a mild temperature range and at lower light levels. Outdoors there are certain times of year when powdery mildew blooms, but greenhouses are always ideal incubators waiting for spores to arrive.

For control of powdery mildew on grapevines, great quantities of sulfur and fungicides are sprayed, the most for any pathogen. However, since weed is newly legalized and gets smoked, growers don’t have an arsenal of chemicals registered for use on it. Cannabis pathologist Zamir Punja from British Columbia has found a few treatments to be effective, including Regalia, which is an extract of giant knotweed, Milstop, which is similar to baking soda but without the sodium, and germicidal ultraviolet light for a few seconds a day. There are some biocontrols that show promise as well. These mostly produce inhibitory chemicals or destructive enzymes against the fungus, or prime the plant to fight off infection, but a recent study from Hungary led by Márk Németh working in the lab of Levente Kiss shows the potential of a biocontrol agent that acts like a creature from science fiction.

In John Carpenter’s 1982 re-visioning of the sci fi classic The Thing, there is not monster played by a man in a suit as in the original, but instead a shape-shifting menace that lives inside its victims, compelling them to act in ways that benefit this alien life form while they retain their own personality. The most riveting scene is where the Kurt Russell character uses a flamethrower to kill a crew member carrying the parasite, which had revealed itself when it had burst out of his chest to engulf the arms of a comrade. The carrier is lying on a table as the flames sear his body, but his head hanging over the edge is out of direct exposure. To the horror of the crew and the audience alike, the head grows a stalk to lower itself to the ground then sprouts legs and tries to slink away. The film proceeds with an air of paranoia as crew members try to figure out who else may be harboring the monster.

The Thing was inspired by the atmosphere of fear and suspicion associated with the cold war, as were many if not all classic sci fi movies, but it could have been inspired by Ampelomyces. This fungus lives inside the tiny threads that make up the powdery mildew. It doesn’t kill the host fungus at first, but grows inside it, finally hijacking its reproductive structures to make more Ampelomyces. The tiny powdery mildew spores become filled with the even tinier spores of the hyperparasite, so-called because it is a parasite of a parasite.

The basic life history of Ampelomyces has been known since the nineteenth century, but Németh et al. have done the definitive study by engineering this fungus to glow green under blue light, allowing them to see its diminutive threads inside its host. They accomplished this using a gene from a jellyfish and a bacterium from a plant gall. The jellyfish is the bioluminescent crystal jelly of Puget Sound, which has a gene for producing green fluorescent protein. The bacterium is the pathogen responsible crown gall in plants, and it alters the growth of its host by inserting a plant tumor gene into the host’s DNA. The scientists replaced the bacterium’s tumor gene with the green fluorescent protein gene, added the bacterium to the fungus culture, and created the green-glowing fungus they were seeking.

One of the key questions that could be answered with an easily seen fungus was, what happens to it outside its host? It turns out that it can survive on a leaf surface for weeks after germination before any host comes along. Considering how utterly tiny the hyperparasite is, and the fact that it is not eating during that time, this is quite a feat. This feature is advantageous for harnessing it as a biocontrol agent, as a grower would not have to wait until a plant is suffering from a powdery mildew infestation to apply Ampelomyces spores. With some appropriate greenhouse trials this might become an additional tool in the pot grower’s toolbox.

Németh et al. also confirmed previous work showing that, unlike powdery mildew, Ampelomyces is not specific to a single host species, but is able grow within many different species of powdery mildew. This feature might make it amenable to conservation biocontrol, where the biocontrol agent is not raised commercially and sprayed onto the crop, but rather the agroecosystem is managed in such a way that hosts are always available for the biocontrol agent to survive on site. Perhaps a grower could leave sowthistles growing around the perimeter of the system to protect the pumpkins. Perhaps the rosebushes at the ends of the grapevine rows could serve not as early warnings for spray timing, but as reservoirs of biocontrol fungus. Further study is required.

And so Jonathan Swift’s observation rings true: “…a Flea/ Hath smaller Fleas that on him prey,/ And these have smaller yet to bite ’em,/ And so proceed ad infinitum…”. Powdery mildew will always be around, but for Ampelomyces that’s a good thing.

Your turn

If you found value in what you have read on this site, feel free to return the favor with a small financial contribution. As of January 2023 I have no other source of income. Clicking on the picture will take you to PayPal. If you are on the single-article page, you can also scroll down to join the conversation.