--Craig Echt and Art Trese

The lesion mutations of maize were first described as "disease lesion mimic mutations" (Neuffer and Calvert, J. Hered. 66:265) because of the striking similarity of their phenotype to pathogen-induced disease lesions on leaves. This morphological similarity has prompted speculation about the role of the lesion mutant loci in plant disease but evidence for a functional connection between lesion mutant and disease expression has been lacking.

We have found that when certain fungal pathogens infect lines segregating Les1 the Les1 allele enhances hyphal growth immediately following infection. Les1 does not, however, alter the basic compatibility (susceptibility) or incompatibility (resistance) interactions determined by the major resistance loci. If Les1 is a mutation in a locus that normally functions in limiting pathogen growth early in the infection process then this function appears to act separately from the pathogen growth-limiting functions of the major resistance loci.

Inoculation of sibling seedlings from several Les1 lines with Bipolaris maydis race O, Cochliobolus heterostrophus race 1 or 2, or Exserohilum turcicum race 1 or 2 showed that the Les1 allele could change an incompatible interaction, giving small chlorotic or necrotic flecks, into a pseudo-compatible interaction, giving moderate size necrotic lesions. The necrotic pathogen-induced lesions that formed on +/Les1 plants appeared within 16h following inoculation and enlarged until about 24h following inoculation. For those line-isolate combinations that resulted in a fully compatible interaction on the +/+ sibs the interaction on the +/Les1 sibs was identical after a period of time (several days to two weeks depending on the pathogen). The reaction types of the various line-isolate combinations tested are given in Table 1. Note that the increased growth of C. het-erostrophus race 1 observed on Les1 plants occurred even in the presence of a defined dominant resistance factor, Hm1 (present in the Pr1 line) but that there was no difference between Les1 and normal plants in the compatible combination (with the Pr line). The same appears to be true for E. turcicum race 2 although the presence of the Ht2 allele in the Pr1 inbred has not been confirmed.

Two observations argue that the larger lesions on infected Les1 plants are not simply due to wound induction of Les1 expression. First, the enhanced disease reactions can occur on leaf sections which are too young to form genetic lesions and which are not yet responsive to wound induction. The second observation is the fluorescence staining of the fungal hyphal structures at the lesion sites showed that the larger disease lesions on +/Les1 plants infected with C. heterostrophus race 1 were correlated with increased hyphal growth. For all disease lesions examined the hyphal growth extended to or just beyond the borders of the necrotic areas. The histology of lesions resulting from other pathogens is currently being examined.

Preliminary experiments with environmental conditions indicate that when conditions inhibitory to normal Les1 lesion formation (30 C or darkness) are employed immediately following inoculation then the differences between +/+ and +/Les1 sibs are not expressed. High temperatures prevent necrotic disease lesion formation while darkness results in increased pathogen growth and lesion size.

The necrotic lesion reactions observed in the Les1-E. turcicum combinations is a novel reaction type for E. turcicum infections on maize. All previously reported maize-E. turcicum interactions, whether ultimately compatible or incompatible, are initially expressed as chlorotic flecks within the first two days after inoculation (Hilu and Hooker, Phytopath. 55:189). Susceptible plants then give rise to long, spreading necrotic lesions about two weeks after inoculation.

Initial whorl inoculations with Colletotrichum graminicola did not elicit larger disease lesions on Les1 plants. The effect of Les1 on pathogen development may be specific to certain groups of pathogens.

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