A porphyrin pathway impairment is responsible for the phenotype of a dominant disease lesion mimic mutant of maize

被引:200
作者
Hu, GS
Yalpani, N
Briggs, SP
Johal, GS [1 ]
机构
[1] Univ Missouri, Dept Agron, Columbia, MO 65211 USA
[2] Pioneer Hi Bred Int Inc, Johnston, IA 50131 USA
关键词
D O I
10.1105/tpc.10.7.1095
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
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页码:1095 / 1105
页数:11
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