Submitted to: Phytopathology
Publication Type: Peer reviewed journal
Publication Acceptance Date: 12/11/2006
Publication Date: 5/1/2007
Publication URL: http://www.apsnet.org/phyto/SubscribeContent/2007/PHYTO-97-5-0584.pdf
Citation: Bennett, R.S., Milgroom, M.G., Sainudiin, R., Cunfer, B.M., Bergstrom, G.C. 2007. Relative Contribution of Seed-transmitted Inoculum to Foliar Populations of Phaeosphaeria nodorum. Phytopathology. 97:584-591. Interpretive Summary: The fungus Phaeosphaeria nodorum is responsible for causing Stagonospora nodorum blotch (also called glume blotch), a major foliar disease of wheat and barley worldwide. In many areas P. nodorum is consistently the predominant foliar pathogen and few effective and affordable controls for this disease exist. There are several sources of inoculum but the relative importance of these sources is not well understood. This study was undertaken to determine the contribution of infected seed relative to airborne inoculum to disease epidemics in a rotational winter wheat system. We found that seed-borne inoculum constituted 31-78% of the recovered isolates of P. nodorum, meaning that 22-69% of the population came from airborne sources. Control plots planted with uninfected seed also became diseased. These results show that strategies focusing solely on seed health will not provide adequate disease control of P. nodoroum epidemics, and that a management approach integrating plant resistance and/or foliar fungicides is needed.
Technical Abstract: A marked-isolate, release-recapture experiment was conducted to assess the relative contributions of seed-transmitted (released isolates) versus all other inocula to foliar and grain populations of Phaeosphaeria nodorum in winter wheat rotated with nonsusceptible crops in New York and Georgia, USA. Seed infected with two distinct groups of marked isolates of P. nodorum containing rare alleles (identified by amplified fragment length polymorphisms, AFLPs) and balanced for mating type were planted in experimental field plots in two locations in each state. Recapture was done by isolating P. nodorum from leaves showing necrotic lesions at spring tillering and flowering stages, and mature grains from spikes showing glume blotch. Isolates from these samples were genotyped by AFLPs and categorized as released or non-released to infer sources of inoculum. Both infected seed and other sources of the pathogen contributed significant primary inocula to populations recovered from leaves and harvested grain. Seed-transmitted genotypes accounted for a range of 31-78% of the populations of P. nodorum collected over the season in inoculated plots at the four locations. Plants in the non-inoculated control plots also became diseased and 95% or more of the isolates recovered from these plots were non-released genotypes. Parental exclusion analysis suggested that the non-released genotypes recovered from inoculated plots were not likely to be recombinant progeny from the released genotypes. The frequency of putative recombinant isolates was not different between treated plots and the background population. Non-released genotypes may have been derived from immigrant ascospores or other airborne fungal propagules, potentially from sources at a considerable distance from the plots. However, other potential sources of P. nodorum within and adjacent to the experimental plots were not ruled out. Our results suggest that while reduction of seedborne inoculum of P. nodorum may delay foliar epidemics, this strategy by itself is unlikely to result in high levels of control in eastern North America because of the additional contribution from alternative sources of inoculum.