Pale-green phenotype of atl31atl6 double mutant leaves is caused by disruption of 5-aminolevulinic acid biosynthesis in Arabidopsis thaliana

• Published in: PloS one Vol. 10; no. 2; p. e0117662
• Main Authors: Maekawa, Shugo, Takabayashi, Atsushi, Huarancca Reyes, Thais, Yamamoto, Hiroko, Tanaka, Ayumi, Sato, Takeo, Yamaguchi, Junji
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science (PLoS) 2015
• Subjects: Aminolevulinic Acid - metabolism; Arabidopsis - genetics; Arabidopsis - metabolism; Arabidopsis Proteins - genetics; Chlorophyll - genetics; Down-Regulation - genetics; Gene Expression Regulation, Plant - genetics; Mutation - genetics; Phenotype; Plant Leaves - genetics; Plant Leaves - metabolism; Plastids - genetics; Thylakoids - genetics; Transcription Factors - genetics; Transcription, Genetic - genetics; Ubiquitin-Protein Ligases - genetics
• DOI: 10.1371/journal.pone.0117662

Arabidopsis ubiquitin ligases ATL31 and homologue ATL6 control the carbon/nitrogen nutrient and pathogen responses. A mutant with the loss-of-function of both atl31 and atl6 developed light intensity-dependent pale-green true leaves, whereas the single knockout mutants did not. Plastid ultrastructure and Blue Native-PAGE analyses revealed that pale-green leaves contain abnormal plastid structure with highly reduced levels of thylakoid proteins. In contrast, the pale-green leaves of the atl31/atl6 mutant showed normal Fv/Fm. In the pale-green leaves of the atl31/atl6, the expression of HEMA1, which encodes the key enzyme for 5-aminolevulinic acid synthesis, the rate-limiting step in chlorophyll biosynthesis, was markedly down-regulated. The expression of key transcription factor GLK1, which directly promotes HEMA1 transcription, was also significantly decreased in atl31/atl6 mutant. Finally, application of 5-aminolevulinic acid to the atl31/atl6 mutants resulted in recovery to a green phenotype. Taken together, these findings indicate that the 5-aminolevulinic acid biosynthesis step was inhibited through the down-regulation of chlorophyll biosynthesis-related genes in the pale-green leaves of atl31/atl6 mutant.