Christopher Lyons

Mundt provides a thorough review detailing the experimental and theoretical usefulness of crop mixtures (i.e. multiline cultivars and cultivar mixtures) in dealing with particular disease and pathogen management issues associated with modern agricultural practices. Within his 2002 Annual Review of Phytopathology paper: Use of Multiline Cultivars and Cultivar Mixtures for Disease Management, Mundt analyses the many research results, shown in the field, in the greenhouse, or in silico that have played important roles in providing evidence of the need for crop diversification strategies and how the use of planting multiline mixtures can successfully function as one of these strategies.

Mundt begins his review with a definition of multiline cultivars and cultivar mixtures. Multiline cultivars he defines as being mixtures of lines bread for phenotypic uniformity of agronomic traits, while he defines cultivar mixtures as blends of agronomically compatible cultivars with no additional breeding for phenotypic uniformity. His definitions depend on the agronomical value of the mixtures in allowing for mutual growth of all its constituents when grown in typical proximity of other members. His definitions also depend on the selective breeding ability of those constituent members (e.g. between constituent members (intra) with viable offspring of “increasing” variability—which itself can result in a propensity for diversity bottlenecking over time, neutral (inter)breeding, and/or (inter/intra)breeding (resulting-in) sterility).

He continues in reiterating a fact shown previously to be valid. There exists a spectrum of “functional diversity”— that is, not all mixture use will result in the same disease reductions. The effects of the particular mixture and, as an extension, the resistance genes contained within that mixed population are dependent on a number of pathogen, pathovar, race, cultivar, environmental, and chance disease-causing/permitting component interactions.

Next, Mundt looks to describe a number of studies regarding the effects of small grain mixture use in the battle again specialized foliar pathogens, such as powdry mildews and rusts. These two main pathogens of wheats and rices, seemingly are controlled through multiline-associated/resultant actions/occurrences, which he calls, dilution of inoculum—which occurs due to increased distances between member plants of the same genotype (which physically separate those member possibly susceptible to infection), induced resistance—which occurs due to plant-to-plant volatile signaling, and race-specific resistance—which means that these mixtures innately contain a multitude of differentiated R-genes and associated alleles which confer resistance to multiple pathogens/pathovars at varying degrees. However, for any diversity that is functional thanks to these characteristics, there will hypothetically exist ways for the pathogen population to evolve to meet these challenges to their growth and propagation. For example, race-specific resistance in hosts does have its disadvantages. There is the possibility that the avirulence genes present in the pathogen population, targeted by the resistance genes existent in the hosts, may be lost as the pathogen population dynamics change over time. The avirulence gene loss may allow for the pathogen population to once again colonize the host cultivar mixes, therefore, statistical approaches must be used in choosing the essential R-genes (whether they are of so-called “high quality” variety or of general value use) represented within the genotypes of the mixture populations. Generally, Mundt contends that “the disease severity will decrease with the decreasing frequency of a host genotype in mixture”—a belief he supports with the quoting of a number of in-field research trials.

Mundt continues in describing a number of other components of the multiline system, which he supports as being essential to their affective use. However, in what I believe is a clear problem in determining the efficiency and validity of claims made under this paradigm, he himself notes the variable experimental procedure controls and design failures that exist in many of the research case-studies. There are also theoretical distinctions he notes about the nature of disease spread (e.g. the epidemiological spread of disease as a mathematical model), that render differencing opinions as to the true nature of disease dynamics and the affectability of multiline use in both in silico simulations and real field studies (of who’s results’ validity statuses are affected by the procedural controls and design problems mentioned before).