The interaction between Helminthosporium carbonum and maize: Induced resistance and the role of an inhibitor

Frank Anthony Cantone, Purdue University

Abstract

Helminthosporium carbonum race 1 produces large, necrotic lesions on susceptible leaves of maize, whereas race 2 causes small, chlorotic flecks. Resistance to race 1 on susceptible leaves was induced when race 2 was inoculated for at least 10 h prior to a challenge inoculation with the pathogen and was manifest as a decrease in the number of appressoria and reduced penetration by race 1 conidia. Induced resistance was prevented or reversed when HC-toxin (a host-specific toxin produced by race 1) was added to challenge race 1 inoculum. The basis for protection appears to be a volatile, inhibitory compound produced by the host. This inhibitor was always associated with treatments that resulted in resistance (i.e., race 2 or race2/race1), whereas no inhibitory activity was detected in diffusates from susceptible reactions (i.e., race 1). The appearance of inhibitor in diffusates coincided with the appearance of protection on the leaf. In addition to race 2 of H. carbonum, other fungi (H. victoriae, H. turcicum, and Alternaria) also induced production of the inhibitor as well as resistance to race 1. The inhibitor prevented the germination of conidia of all fungi tested. The growth of two phytopathogenic bacteria was also completely inhibited. Incorporation of $\sp3$H-leucine and $\sp{14}$C-uridine into protein and RNA, respectively, by conidia of H. carbonum was prevented within 15 min of exposure to inhibitor. In addition, respiration of conidia in inhibitor was reduced within 90 min to just 25% of the rate of conidia germinated in water. However, inhibitory activity of the diffusates was readily reversed when conidia were rinsed with water or when organic or amino acids were added to inhibited conidia. The addition of sodium acetate to race 2 and race 1 inocula resulted in lesion enlargement and also nullified inhibitory activity in vitro. HC-toxin was recovered from diffusates and from tissue infected with race 1 at 12 and 18 h, respectively. The role of HC-toxin in this interaction is unclear, since it does not alter the affectivity of the inhibitor in vitro, but toxin is likely involved in preventing the synthesis of the inhibitor or indirectly affecting its activity in vivo.

Degree

Ph.D.

Advisors

Dunkle, Purdue University.

Subject Area

Plant pathology

COinS