Loss of the plastid envelope protein AtLrgB causes spontaneous chlorotic cell death in Arabidopsis thaliana.

To identify nuclear genes involved in plastid function, we analyzed Arabidopsis thaliana mutants with albino, pale green or variegated leaves using the Activator/Dissociation (Ac/Ds) transposon tagging system. In this study, we focused on mutants with a Ds insertion in the gene At1g32080 (AtLrgB), which encodes a homolog of the bacterial membrane protein LrgB. Although the detailed function of bacterial LrgB remains unclear, it is speculated that LrgB functions against cell death and lysis in cooperation with LrgA. Reverse transcription-PCR (RT-PCR) and promoter-GUS (β-glucuronidase) analyses showed that AtLrgB is expressed in leaves, stems and flowers, but not in roots. Moreover, its expression in leaves continued until senescence. We used three Ac/Ds-tagged mutants (atlrgB) that showed the same phenotypes. During the continuous observation of seedlings under short-day conditions, we found that the cotyledons and true leaves of the mutant plants during early development showed immediate greening, similar to wild-type plants, after which some parts showed a chlorotic phenotype. In contrast, true leaves at the late stage of plant development did not show degreening. When the atlrgB mutant was grown under continuous light, its chlorotic phenotype was suppressed. Transformation with normal AtLrgB restored these phenotypes. Trypan blue staining and electron microscopic observations indicated that chlorotic cell death occurred in the white sectors. The phenotypes of atlrgB resembled those in lesion mimic mutants, suggesting that AtLrgB functions against cell death, similar to the bacterial Lrg system.