Author
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Lulai, Edward |
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Submitted to: American Journal of Potato Research
Publication Type: Peer Reviewed Journal Publication Acceptance Date: 3/22/2000 Publication Date: N/A Citation: N/A Interpretive Summary: The periderm on the surface of a potato tuber provides a durable barrier to resist penetration by pathogens. However, other disease resistance responses, such as the induction of plant antimicrobials called phytoalexins, must be elicited to deter infection through wounds created during harvest and seed cutting. Despite the importance of phytoalexins, little is known about how the different types of tissues within the tuber respond to stimulation for phytoalexin accumulation to resist disease. We elicited accumulation of phytoalexins in tuber wounds and various isolated tuber tissues using arachidonic acid, a commercially available fungal component known to induce phytoalexin synthesis. The accumulation of rishitin, the most prominent tuber phytoalexin, was monitored to serve as a model for overall phytoalexin induction. Elicitor treated wounds on/near the surface of the tuber accumulated little rishitin. Deeper, more severe tuber wounds accumulated significant amounts of rishitin. Isolated cortical tissues from potato accumulated more rishitin than isolated perimedullary and pith tissues. Over 80% of the rishitin was accumulated within 0.75 mm of the treated wound indicating a very localized resistance response. The results are important because they: 1) demonstrate a tissue based differential within the potato tuber which influences the induction of host resistance to pathogens, and 2) show that the tuber tissue disk model system, often used in research, may simulate the rishitin accumulation response in cut tubers such as those used for seed, but the disk system may not be valid for simulating a phytoalexin response in wounded intact tubers. Technical Abstract: The wound response within damaged tubers must be a coordination of suberization with other resistance responses if infection is to be avoided. Previously, we showed that wound healing was affected by wound severity and consequently the type of tissue damaged within the tuber. Using arachidonic acid induced accumulation of rishitin as a model for phytoalexin accumulation, we now demonstrate that this tuber resistance response is also influenced by wound severity and the type of tissue exposed to the elicitor. Kennebec and Reddale tubers that were wounded by removing a thin tissue slice (0.75mm thick) from the surface and then treated with the elicitor arachidonic acid produced significantly less rishitin than more severely wounded tubers (e.g. tubers cut in half) and excised tuber tissue disks (17mm x 4mm). Excised, elicitor treated tuber tissues accumulated significantly more rishitin in cortical cells than perimedullary and pith cells. Rishitin accumulation was routinely measured 96 hr after wounding and was found to be declining by 144 hr regardless of wound severity. Induction of rishitin accumulation was very localized with over 80 % of the rishitin found within 0.75mm of the treated wound. These results indicate that excised tuber tissue disks, used as models in wound research, are not fully representative of intact tubers and that superficially wounded intact tubers do not accumulate phytoalexins to the same extent as that found in the standard tuber disk models. The complications contributed by these wound related and tissue specific interactions must be factored into the model system(s) used in describing the role(s) of phytoalexins in the broad framework of disease resistance for stored potatoes and cut seed. |
