PHYSIOLOGICAL STUDIES ON A NECROTIC MUTANT OF CORN

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Abstract
The leaves of homozygous nec. 1 plants (a single-gene, necrotic maize mutant) develop visible necrotic symptoms when they are exposed to light for several days. Extensive analysis has failed to reveal any difference in chemical composition between leaves of normal plants and of homozygous nec. 1 plants before the necrotic symptoms are visible (prenecrotic leaves). Treatment of nec. 1 seedlings with various metabolites (B vitamins, purines, pyrimidines, amino acids, etc.) did not prevent the appearance of necrosis. The rate of photosynthesis of prenecrotic leaves is normal at low light intensities but only 20 to50% of normal at saturating light intensity. C14O2 feeding experiments indicate that the photosynthetic carbon-fixing reactions function normally in the mutant. Hill reaction rates are also similar in mutant and normal plants, as is the metabolism of labelled inorganic phosphate. 3-(p-Chlorophenyl)-1,1-dimethylurea, which specifically inhibits photosynthesis to the extent of about 90%, delays the onset of visible necrotic damage and reduces the severity of subsequent necrotic symptoms. It is suggested that the basic lesion in nec. 1 plants lies in a reaction associated with photosynthesis and that it causes the accumulation of one or more toxic substances. These materials lower the rate of photosynthesis and damage cell membranes. The necrotic phenotype would appear to be the result of the breakdown of cell compartmentalization.