Disease lesion mimics
--Guri Johal* and Steve Briggs
*New Address: University of Missouri, Columbia, Missouri

Disease lesion mimics are a class of mutants that promote the production of discrete leaf lesions in the absence of obvious stress, injury or disease on the plants. These are named disease lesion mimics because each mutation causes symptoms that resemble some known pathological condition of maize (Walbot, V, Hoisington, DA and Neuffer, MG, in Genetic Engineering of Plants, eds. Kosuge et al. p. 431, 1983). Both spontaneous and mutagen-induced cases of recessive and dominant lesion mimic mutations have been reported. A majority of these mutations are dominant. Nothing is known about the nature of these mutations, but it is likely that they represent defects in either the plant's recognitional system or in mechanisms that regulate symptom development during infection.

Lesion mimics constitute excellent models for plant cell-cell interactions. Three issues can be directly addressed by cloning and characterizing lesion genes: how are signals initiated, propagated, and terminated? The large number of mutants in maize suggests that there may be pathways for lesion development. This should be a fruitful avenue for genetic investigation. While such studies are of a basic nature, they have the added value of potentially elucidating the process of infectious disease development.

We are particularly interested in lethal leaf spot (lls1), a recessive mutation which mimics the symptoms produced by race 1 of H. carbonum on susceptible maize (Ullstrup and Troyer, Phytopathology 57:1282, 1967). The expression of lls1 is developmentally programmed; there is a progression of lesion formation, beginning first in the most mature and advancing toward the youngest tissues. Lesions first appear near the tips of the oldest leaves about three weeks after seedling emergence and then spread and enlarge to kill the plant just before or shortly after pollen shed. Thus, the developmental distribution of lesions on the plant, as well as the development and appearance of individual lesions, mimics closely disease caused by H. carbonum race 1.

A project has been initiated to tag lls1 with Mutator (Mu). Both the targeted and random-mutagenesis approaches were taken. Seven Mu-induced alleles (including two that are mutable) have been isolated. These mutants have been advanced three generations and are now ready to be subjected to cosegregation analysis.

In the course of this and the Hm1 cloning project, 16 cases of a dominant lesion mimic mutation, designated Les*-2552, were recovered from Mutator lines. Phenotypically they all look alike, and four of them have been shown to be allelic. This mutation differs from lls1 in that the lesions are arrested in their growth while still small (~1mm). A number of these Les*-2552 alleles have been advanced 3-4 generations to reduce the number of background Mu elements.

Both lls1 and Les*-2552 are cell-autonomous. Somatic clonal sectors were observed either as forward mutations or reversion events for both mutations. These sectors may be the result of somatic transposition of Mu during development. A cloning strategy based on the use of these mutant sectors is under investigation. Briefly, the Mu-hybridization pattern of DNA from a mutant sector is compared with the DNA from adjacent wildtype tissue. Any extra band in the mutant DNA may represent the Mu insertion responsible for the mutation. Using this approach, a Mu1 hybridizing 6.0kb fragment was identified from the lls1-1424 mutant and association of this restriction fragment with the mutant allele was confirmed by cosegregation analysis in progeny derived from this mutant. To incite early (large) revertant sectors, which will be critical for the strategy outlined above, both lls1 and Les*-2552 mutants have been crossed with Ginny Walbot's 'big spot' Mutator line carrying bz2-Mu2 (MNL65:96, 1991). 


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