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ARS Home » Midwest Area » St. Paul, Minnesota » Cereal Disease Lab » Research » Publications at this Location » Publication #69824
Title: ISOLATION AND EXPRESSION OF HOST RESPONSE GENES ASSOCIATED WITH RESISTANCE IN OAT AGAINST PUCCINIA GRAMINIS

Author
item LIN, KUO-CHIH - UNIVERSITY OF MINNESOTA
item Bushnell, William
item Szabo, Les

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 7/14/1996
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Resistance in oat (Rodney, Pg-2) to an incompatible isolate (Pga-1H) of P. graminis f.sp. avenae was expressed by retardation of fungal growth by 42-48 hr after inoculation (AI) and by hypersensitive cell death (HCD), which occurred at 6% of the infection sites at 36 hr AI, 15% at 42 hr AI, and increased to 30% by 72 hr AI. Six cDNA clones were isolated from a cDNA library prepared from infected resistant leaves at 36-60 hr AI. Four of the clones (tlp-1, -2, -3 and -4) were homologous with genes encoding thaumatin-like proteins. The 5th clone was homologous with genes for a key enzyme in glycolysis, 3-phosphoglycerate kinase (3-PGK). The 6th clone (pCRL120) had no homology with known genes. RNA blot analyses showed that inoculation procedures induced a temporary peak in transcript levels of tlp-1, -2, -3 and pCRL120, obscuring possible induction by fungal infection at 16-24 hr AI. By 30 hr, however, 3-PGK and pCRL120 were induced preferentially in the incompatible interaction, before resistance was expressed by either HCD or fungal growth retardation. By 36 hr AI, tlp-4 was also induced preferentially. By 42 hr AI, tlp-1, -2 and -3 were also expressed preferentially, at the time when inhibition of fungal growth was first detected. The results indicate that 3-PGK and pCRL120 were induced prior to detectable retardation of pathogen growth or HCD and that the other genes were induced just preceding or in the early stages of the resistance reaction. This, in turn, suggests that all six genes were activated in association with physiological events leading to resistance, not as a secondary consequence of the resistance reaction.