A deficiency of coproporphyrinogen III oxidase causes lesion formation in Arabidopsis

Ishikawa, A Okamoto, H Iwasaki, Y Asahi, T

A. Ishikawa et al., A deficiency of coproporphyrinogen III oxidase causes lesion formation in Arabidopsis, PLANT J, 27(2), 2001, pp. 89-99

59

INGLESE

Article

Plant Sciences","Animal & Plant Sciences

PLANT JOURNAL

0960-7412 → ACNP

27

2

2001

89 - 99

ISI

0960-7412(200107)27:2<89:ADOCIO>2.0.ZU;2-V

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.