Canker pathogens cause necrosis of the phloem, but in many host/pathogen systems, they also cause canopy dieback, which implicates xylem, not phloem dysfunction. We hypothesize this dieback distal to the… Click to show full abstract
Canker pathogens cause necrosis of the phloem, but in many host/pathogen systems, they also cause canopy dieback, which implicates xylem, not phloem dysfunction. We hypothesize this dieback distal to the canker is caused by water stress resulting from the lack of a phloem-to-xylem connection, which in a healthy plant would allow delivery of nonstructural carbohydrates (NSCs) and water inward to aid in xylem embolism refilling. We tested several components of this hypothesis in the host/pathogen system Corylus avellana L./Anisogramma anomala (Peck) E. Müll (Eastern filbert blight). Cankers were non-girdling, and usually ≥0.1 m long. As expected, healthy controls had higher specific conductivity (Ks) than diseased stems, but unexpectedly, had similar moisture content (m.c.), showing that the lower Ks did not result from more embolisms in the diseased stems. Moreover, manipulations that removed cambium and phloem to simulate a canker, or that shaded stems to lower NSCs, did not result in lower Ks or m.c. than controls. The outer millimeter of xylem adjacent to a canker had infrequent tyloses and/or fungal hyphae in many but not all samples, and dye studies showed little xylem water transport in that region, but the incidence of these blockages was insufficient to cause the observed 19% decrease in Ks. Healthy stems had higher m.c. than diseased stems above the canker (or analogous) location, and were longer for the same leaf weight, suggestive of water stress in the upper portion of diseased stems. These results suggest that dieback distal to cankers in this system results from the bottleneck in water transport in the region adjacent to a canker, but did not find evidence to support the requirement of a phloem-to-xylem connection for continued water transport.
               
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