Genetic variation among plants has the potential to alter many aspects of the habitat shared by pathogens and non-pathogenic endophytes, which together comprise the plant-associated microbiome. Currently, however, the links between host genotype, microbiome composition, and pathogen success are poorly understood.
To address this problem, we used germplasm from a real maize breeding population to compare microbiome composition and diversity before and after introgression of broad-spectrum disease resistance genes. We planted 11 inbred maize lines in four fields near Raleigh, NC and quantified their foliar fungal and bacterial communities using deep rDNA amplicon sequencing. Eight of these genotypes were near-isogenic lines that were ~80-95% genetically identical to a highly disease-susceptible parent line, but with introgressed genome regions from a highly MDR parent that conferred partial resistance to three diverse fungal pathogens. By comparing microbiome composition of these near-isogenic lines to that of their disease-susceptible parent line, we tested the effects of various MDR loci on the establishment of non-pathogenic microbes in maize leaves. We sampled all plants as seedlings, and again later in the season after inoculation with one of two maize pathogens (Cochliobolus heterostrophus or Exserohilum turcicum).
Results/Conclusions
A pilot study revealed that disease-resistant maize plants harbored leaf fungal communities that were over 30% more diverse, on average, than those of disease-susceptible plants. Microbiome diversity of near-isogenic lines was generally intermediate to that of the parent lines. In addition to affecting overall microbiome diversity, disease-resistance loci increased or decreased abundance of >16% of microbiome members by 16-fold, on average.
We will discuss results from an expanded replication of this experiment, presenting data from four fields and two timepoints (before and after disease inoculation, or seedling and adult stages for non-inoculated controls). This dataset will enable us to address questions such as: Does host genotype directly affect both early- and mid-season microbiome composition, both in the presence and absence of pathogens? Does early-season microbiome composition predict future disease severity? Do different pathogens disrupt microbiome structure in similar ways? Our results will shed light on how pathogenic and non-pathogenic microbiome members respond to host genetic variation affecting their shared environment.