Abstract
Lesion mimic mutants develop spontaneous cell death without pathogen attack. To understand the molecular mechanism of cell death in lesion mimic mutants, we isolated len1 and lin2 mutants. The len1 mutant develops lesions on its leaves under short-day conditions. LEN1 was identified to encode a chloroplast chaperonin 60b (Cpn60b), a homologue of bacterial GroL. However, we do not know the mechanism of the lesion initiation of len1 plants. The lin2 mutant develops lesion formation on leaves and siliques in a developmentally regulated and light-dependent manner. LIN2 encodes coproporphyrinogen III oxidase, a key enzyme in the biosynthetic pathway of chlorophyll and heme, a tetrapyrrole pathway, in Arabidopsis. The len1lin2 plants showed reduced lesion formation than len1 plants under short-day conditions. This would suggest that LIN2 would be necessary to execute lesion formation in len1 plants.
