--C. W. Roane and S. A. Tolin

In our paper on inheritance of reaction to maize dwarf mosaic virus (MDMV) in crosses of the resistant inbred line Oh7B with two susceptible lines (Roane, Tolin and Genter, Phytopathology 73:845-850, 1983), we described a scale for recording the symptoms induced by the virus. Our scale had 7 categories. Here we are concerned with reaction types 2, 3, and 4. In type 2 plants, narrow stripes of mosaic tissue occur on leaves below the ear; in type 3 plants, narrow stripes occur in leaves above the ear; and in type 4 plants, narrow stripes occur in leaves above and below the ear. We reported that nine F2 plants scored in the 2 to 4 range. Upon selfing, in F3 two plants were homozygous resistant, six were considered heterozygous and one produced a majority of susceptible plants. Prior to our report, plants with any expression of symptoms had been regarded as susceptible but we took the approach that if a plant restricted the development of symptoms, it must have some resistance and restrict replication or movement of the virus. We also suggested that striping might occur in resistant plants if somatic mutations for susceptibility occurred early in plant development to produce cells which permitted virus replication. If this were true, striping might conform to the fate map concept proposed by Walbot et al. (Proc. 34th Annual Corn and Sorghum Conf. 92-103, 1979). To gain evidence for somatic mutations, in 1985 we selfed a number of plants in some breeding lines which displayed symptoms in the 2-4 range. Type 2 and 4 plants were of special interest because the susceptible tissue might also extend into the ear. If such were the case, by dissecting ears such that pairs of kernels originating from the same spikelet and rows of spikelets were harvested as units, we could plant, inoculate and observe to see if a higher frequency of susceptible plants could be obtained from some pairs of kernel rows. Eight type 2 and type 4 plants were selfed. The ears were harvested and dissected and kernels planted as described above. Oh7B was the source of resistance but the plants were of different and complex pedigrees. We expected that, if our assumption that a somatic mutation for susceptibility occurred and extended into the ear, most rows of spikelets would produce a low frequency of susceptible plants and one or two rows of spikelets would produce a high frequency of susceptibles.

The results did not support our assumption. Susceptible plants were randomly distributed and we could find no evidence that a putative somatic mutation extended into the ear. Yet this assumption seems logical to us because the patterns of striping are not random. If blades may be described as left and right in their alternate phyllotaxy, stripes on the right side appear on the same side of the midrib as do those on the left side. In addition, the stripe of mosaic tissue usually extends halfway between adjacent secondary veins, indicating a presence of the virus in particular secondary veins and, consequently, in particular stalk vascular bundles. These should extend into the ear. Our limited observations do not support the assumption but perhaps experiments designed to test the assumption might be more conclusive.

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