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.