Many times growers observe field outcomes we don’t have an immediate explanation for.
Why did that one section of the field with that early root disease not have any insect pressure later in the season?
Why does our crop not have any disease where we foliar fed last years cover crop, but disease is present where the same cover crop was not foliar fed?
Why does a field have greater disease pressure on one variety, but the next variety right beside it, not particularly selected for disease resistance, showed no trace of disease?
Why do GM crops seem to produce a disease conducive soil, where their non GM counterparts produce a disease suppressive soil microbiome?
Why does the relative health and photosynthetic efficiency of crops result in changed microbiomes in the soil?
Then, sometimes, we find a reference that connects the dots, and we learn some possibilities of what might have occured to produce unexpected results.
The Rhizosphere Microbiome and Plant Health is such a paper. Here are some condensed highlights from the paper:
– The microflora of most soils is starved. As a result,there is a fierce battle in the rhizosphere between the microorganisms that compete for plant-derived nutrients.
– Most soil-borne pathogens need to grow saprophytically in the rhizosphere to reach their host.
– The success of a pathogen is influenced by the microbial community of the soil in which the infection takes place.
– Every natural soil has the ability to suppress a pathogen to a certain extent. This phenomenon is known as general disease suppression and is attributed to the total microbial activity.
– Organic amendments can stimulate the activity of microbial populations in a conducive soil, resulting in enhanced general disease suppressiveness.
– ‘Specific suppression’ occurs when specific microorganisms cause soils to be suppressive to a disease. Specific disease suppressiveness is superimposed on the general disease suppressiveness of soils and is more effective.
– some soils retain their disease suppressiveness for prolonged periods and persist even when soils are left bare, whereas other soils develop suppressiveness only after monoculture of a crop for several years.
– Induction of suppressiveness by itself is remarkable, because for most plant species, successive monocultures will lead to a build-up of specialized plant pathogens .
– Nonetheless, development of disease suppressiveness in soils has been reported for various diseases, including potato scab, Fusarium wilt, Rhizoctonia damping-off , and take-all.
– Microorganisms that can confer suppressiveness to otherwise conducive soils have been isolated from many suppressive soils.
– Mechanisms through which rhizosphere microorganisms can affect a soil-borne pathogen have been identified and include production of antibiotic compounds, consumption of pathogen stimulatory compounds, competition for (micro)nutrients and production of lytic enzymes.
– Many beneficial soil-borne microorganisms have been found to boost the defensive capacity in above- ground parts of the plant. This induced systemic resistance (ISR) is a state in which the immune system of the plant is primed for accelerated activation of defense.
– Although locally plant immunity is suppressed, an immune signaling cascade is initiated systemically that confers resistance against a broad spectrum of pathogens and even insects
– In addition to plant growth-promoting rhizobacteria, beneficial fungi such as mycorrhizal fungi, Trichoderma spp. and other fungal biocontrol agents have also been found to induce ISR.
– As well as inducing systemic resistance, mycorrhizal fungi can also form a connecting network between plants that can convey a resistance-inducing signal to neighboring plants
– The microflora of most soils is carbon starved. Because plants secrete up to 40% of their photosynthates into the rhizosphere, the microbial population densities in the rhizosphere are much higher than in the surrounding bulk soil.
– From the reservoir of microbial diversity that the bulk soil comprises, plant roots select for specific microorganisms to prosper in the rhizosphere.
– Some plant species can create similar communities in different soils. Even within species, different genotypes can develop distinct microbial communities in the rhizosphere, suggesting that plants are able to shape the composition of the microbiome in their rhizosphere.
– Plants can determine the composition of the root microbiome by active secretion of compounds that specifically stimulate or repress members of the microbial community
– Furthermore, plant-associated bacteria produce and utilize diffusible N-acyl-homoserine lactones (AHLs) to signal to each other and to regulate their gene expression. Such cell-to-cell communication is known as ‘quorum sensing’
– QS-interfering compounds enable the plant to manipulate gene expression in their bacterial communities
– Recent evidence suggests that differences between plant genotypes in a single gene can have a significant impact on the rhizosphere microbiome. The production of a single exogenous glucosinolate significantly altered the microbial community on the roots of transgenic Arabidopsis.
– These results indicate that the plant genotype can affect the accumulation of microorganisms that help the plant to defend itself against pathogen attack. Indeed, differences have been found in the ability of wheat cultivars to accumulate naturally occurring DAPG-producing Pseudomonas spp., resulting in differences in disease suppressiveness.
– Specific wheat cultivars support specific biological control bacteria differentially, which further establishes that there is a degree of specificity in the interactions between plant genotype and the composition of their microbial community
– White fly feeding also led to significant changes in the rhizosphere microbial community. Although total numbers of bacteria were unaffected, the white fly- induced plants had higher populations of Gram-positive bacteria and fungi in their rhizosphere. The authors hypothesized that plants recruit plant-beneficial microbes to their roots in response to the attack.
