We isolated an Arabidopsis lesion initiation 2 (lin2) mutant, which develop
s lesion formation on leaves and siliques in a developmentally regulated an
d light-dependent manner. The phenotype of the lin2 plants resulted from a
single nuclear recessive mutation, and LIN2 was isolated by a T-DNA tagging
approach. LIN2 encodes coproporphyrinogen III oxidase, a key enzyme in the
biosynthetic pathway of chlorophyll and heme, a tetrapyrrole pathway, in A
rabidopsis. The lin2 plants express cytological and molecular markers assoc
iated with the defense responses, usually activated by pathogen infection.
These results demonstrate that a porphyrin pathway impairment is responsibl
e for the lesion initiation phenotype, which leads to the activation of def
ense responses, in Arabidopsis. Lesion formation was not suppressed, and wa
s even enhanced when accumulation of salicylic acid (SA) was prevented in l
in2 plants by the expression of an SA-degrading salicylate hydroxylase (nah
G) gene. This suggests that the lesion formation triggered in lin2 plants i
s determined prior to or independently of the accumulation of SA but that t
he accumulation is required to limit the spread of lesions in lin2 plants.