6
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Arabidopsis CHLI2 can substitute for CHLI1.

      Plant physiology
      Amino Acid Sequence, Arabidopsis, enzymology, genetics, Arabidopsis Proteins, chemistry, metabolism, Chlorophyll, biosynthesis, Gene Expression Regulation, Plant, Immunoblotting, Lyases, Molecular Sequence Data, Mutation, Phenotype, Promoter Regions, Genetic, Protein Stability, RNA, Messenger

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          The I subunit of magnesium-chelatase (CHLI) is encoded by two genes in Arabidopsis (Arabidopsis thaliana), CHLI1 and CHLI2. Conflicting results have been reported concerning the functions of the two proteins. We show here that the chli1/chli1 chli2/chli2 double knockout mutant was albino. Comparison with the pale-green phenotype of a chli1/chli1 single knockout mutant indicates that CHLI2 could support some chlorophyll biosynthesis in the complete absence of CHLI1. Real-time quantitative reverse transcription-polymerase chain reaction showed that CHLI2 was expressed at a much lower level than CHLI1. The chli1/chli1 chli2/chli2 double mutant could be fully rescued by expressing a transgene of CHLI2 driven by the CHLI1 promoter. These results suggest that differences between CHLI1 and CHLI2 lie mostly in their expression levels. Furthermore, both the chli1/chli1 and chli2/chli2 single knockout mutants had lower survival rates during de-etiolation than the wild type, suggesting that both genes are required for optimal growth during de-etiolation. In addition, we show that a semidominant chli1 mutant allele and the chli1/chli1 chli2/chli2 double mutant accumulated Lhcb1 transcripts when treated with the herbicide norflurazon, indicating that knocking out the CHLI activity causes the genome-uncoupled phenotype.

          Related collections

          Author and article information

          Comments

          Comment on this article