Transgenic rice containing an antisense cDNA for the ␣ subunit of rice heterotrimeric G protein produced little or no mRNA for the subunit and exhibited abnormal morphology, including dwarf traits and the setting of small seeds. In normal rice, the mRNA for the ␣ subunit was abundant in the internodes and f lorets, the tissues closely related to abnormality in the dwarf transformants. The position of the ␣-subunit gene was mapped on rice chromosome 5 by mapping with the restriction fragment length polymorphism. The position was closely linked to the locus of a rice dwarf mutant, Daikoku dwarf (d-1), which is known to exhibit abnormal phenotypes similar to those of the transformants that suppressed the endogenous mRNA for the ␣ subunit by antisense technology. Analysis of the cDNAs for the ␣ subunits of five alleles of Daikoku dwarf (d-1), ID-1, DK22, DKT-1, DKT-2, and CM1361-1, showed that these dwarf mutants had mutated in the coding region of the ␣-subunit gene. These results show that the G protein functions in the formation of normal internodes and seeds in rice.

SummaryWe isolated an Arabidopsis lesion initiation 2 (lin2) mutant, which develops lesion formation on leaves and siliques in a developmentally regulated and 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 Arabidopsis. The lin2 plants express cytological and molecular markers associated with the defense responses, usually activated by pathogen infection. These results demonstrate that a porphyrin pathway impairment is responsible for the lesion initiation phenotype, which leads to the activation of defense responses, in Arabidopsis. Lesion formation was not suppressed, and was even enhanced when accumulation of salicylic acid (SA) was prevented in lin2 plants by the expression of an SA-degrading salicylate hydroxylase (nahG) gene. This suggests that the lesion formation triggered in lin2 plants is determined prior to or independently of the accumulation of SA but that the accumulation is required to limit the spread of lesions in lin2 plants.

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