A recessive disease lesion mimic

A line segregating for an apparent disease lesion mimic was obtained in a program designed to backcross the polymitotic (po) allele into inbred A632 and simultaneously select for improved seed set on male-sterile (po) plants. This line represented the selfed progeny of a fertile plant derived from the open-pollinated progeny of a po plant. This po plant was from the selfed progeny of a fifth backcross of po to A632. The disease lesion mimic mutation was of apparent spontaneous origin because other lines of similar descent did not segregate for the trait.

Plants first show the lesions at about the 9-leaf stage (6 weeks after planting in 1983). Lesions are concentric necrotic spots with alternating light and dark rings; the lesions may stop at a vein. Watersoaked-appearing areas later encompass the lesions. Eventually the entire leaf becomes necrotic. Ear shoots are not apparent; however, tassels are produced and anthers may dehisce and shed viable pollen. Pollen is variable in size and approximately 50% is partially filled with starch. The entire plant ultimately becomes necrotic and degenerates. By 9 weeks after planting, the lower 2-3 leaves are totally necrotic. By 11 weeks, the flag leaf is one-half necrotic, progressively greater necrosis occurs over the next three leaves, and lower leaves are totally necrotic.

No fungal or bacterial microorganisms are specifically associated with the lesions according to moist-chamber tests with isolated leaf segments (pers. commun., Dr. Thor Kommedahl, Department of Plant Pathology, University of Minnesota). Unsuccessful attempts were made to spread the disease to normal siblings by grinding affected leaves in water and placing soaked pipe cleaners through the leaves of normal siblings. Dr. Kommedahl described the lesion phenotype as resembling "target spot." A mutant with a target spot phenotype was reported previously in the 1954 Maize Genetics Coop News Letter (28:29); the trait was controlled by a single recessive allele tentatively located in chromosome 9.

Backcrosses of heterozygous normal plants as female to homozygous disease lesion mimic plants as male produced 73 normal and 67 disease lesion mimic plants. In F2's of crosses with several independent waxy-marked translocations, a total of 532 normal and 216 disease lesion mimic plants were produced. Therefore, the trait is probably controlled by a single recessive allele, although the ratio in F2 is somewhat deviant (P = .01-.05). Further tests to map the gene are underway.

R. L. Phillips
 
 


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