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The lesion nematode, Pratylenchus penetrans, and the fungus, Verticillium dahliae, interact synergistically to cause the potato early dying (PED) disease. My primary research goal was to provide physiological and cytological evidence that the nematode alters host susceptibility to the fungus. My overall experimental approach was to spatially separate the two pathogens on their host in order to distinguish the influence of the nematode on colonization of the vasculature by the fungus and associated host events from the interaction of these two organisms in the roots at their point of entry.
Using a split root system to separate the pathogens, I determined that P. penetrans had a localized influence on the colonization of Russet Burbank stems by V. dahliae when inoculation with the fungus was sufficient to cause disease alone. The number of colony forming units (CFU) of V. dahliae in stems was enhanced when the nematode and fungus physically occupied the same root half in one experiment. Stem colonization was not affected by the nematode when the two pathogens were spatially separated. In a second experiment, the proportion of infected stem vessels was greater when the nematode and fungus occupied the same root half.
By delivering the fungus directly to the stem vasculature of potato predisposed to the nematode, I demonstrated synergistic effects on light use efficiency (LUE) and transpiration when the pathogens occupied different plant organs. The number of CFU of V. dahliae was greater in co-infected potato. At the light microscope level, potato stems colonized by the fungus, regardless of the presence of the nematode, exhibited a reddish-brown discoloration in xylem vessel walls in cross-section. Joint infection resulted in a greater proportion of xylem vessels exhibiting the cytological response to fungal infection. The proportion of discolored vessels correlated with the proportion of infected vessels and LUE in the co-infected plants only. My data indicate that P. penetrans can systemically alter a xylem host response to the fungus, which may play a role in induced susceptibility to the fungus.