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Plant Cell, Vol. 10, 1095-1106, July 1998, Copyright © 1998, American Society of Plant Physiologists

A Porphyrin Pathway Impairment Is Responsible for the Phenotype of a Dominant Disease Lesion Mimic Mutant of Maize

Gongshe Hua, Nasser Yalpanib, Steven P. Briggsb, and Gurmukh S. Johala
a Department of Agronomy, University of Missouri, Columbia, Missouri 65211
b Pioneer Hi-Bred International Inc., 7300 N.W. 62nd Avenue, Johnston, Iowa 50131

Correspondence to: Gurmukh S. Johal, agrogj{at}showme.missouri.edu (E-mail), 573-884-7850 (fax).

The maize lesion mimic gene Les22 is defined by dominant mutations and characterized by the production of minute necrotic spots on leaves in a developmentally specified and light-dependent manner. Phenotypically, Les22 lesions resemble those that are triggered during a hypersensitive disease resistance response of plants to pathogens. We have cloned Les22 by using a Mutator-tagging technique. It encodes uroporphyrinogen decarboxylase (UROD), a key enzyme in the biosynthetic pathway of chlorophyll and heme in plants. Urod mutations in humans are also dominant and cause the metabolic disorder porphyria, which manifests itself as light-induced skin morbidity resulting from an excessive accumulation of photoexcitable uroporphyrin. The phenotypic and genetic similarities between porphyria and Les22 along with our observation that Les22 is also associated with an accumulation of uroporphyrin revealed what appears to be a case of natural porphyria in plants.


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