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ARS Home » Midwest Area » St. Paul, Minnesota » Cereal Disease Lab » Research » Publications at this Location » Publication #59090

Title: INHIBITION OF PHENYLALANINE AMMONIA LYASE (PAL) OR CINNAMYL-ALCOHOL DEHYDROGENASE (CAD) SUPPRESSES ML-A, BUT NOT ML-O RESISTANCE IN POWDERY MILDEW OF BARLEY

Author
item Bushnell, William
item ZEYEN, RICHARD - UNIVERSITY OF MINNESOTA
item CARVER, TIMOTHY - AFRC, IGER, UK
item ROBBINS, M - AFRC, IGER, UK

Submitted to: Journal of Cellular Biochemistry Supplement
Publication Type: Abstract Only
Publication Acceptance Date: 1/1/1994
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: AOPP, an inhibitor of phenylalanine ammonia lyase (PAL) and OH-PAS, an inhibitor of cinnamyl-alcohol dehydrogenase (CAD) were tested for effects on Ml-a and ml-o major gene resistances in powdery mildew of barley. The inhibitors were applied either directly to epidermal tissues dissected from coleoptiles, or through cut ends of detached leaves. With Ml-a, which conditions rapid hypersensitive cell death, both AOPP and OH-PAS strongly inhibited the hypersensitive reaction. The reduction in the hypersensitive response in coleoptile tissue was accompanied by increase in average haustorium size and percentage of germlings that produced hyphae. Furthermore, OH-PAS was effective with coleoptile tissue when applied as late as 16 hr after inoculation, about 2 hr before the beginning of hypersensitive cell death. The results strongly indicate that CAD activity has a direct role in hypersensitive resistance, and suggest that cinnamic acid products of CAD are required. In contrast, ml-o resistance, which is expressed by failure of the fungus to penetrate host cells and form haustoria, was unaffected by OH-PAS or AOPP. These results indicate that ml-o resistance does not require PAL or CAD activity for effectiveness, suggesting, in turn, that ml-o resistance is independent of the phenyl propenoid pathway. Clearly, the resistances due to Ml-a and ml-o differ in underlying physiological mechanisms.