PARENT SESSION

Symposium S6B Photosynthetic acclimation: Mechanisms and gene expression
Thursday September 2nd, 2004 10:20 AM-12:40 PM Room 210A
Chair: Norio Murata
Co-Chair: Eva-Mari Aro

Mutational analysis of atProRS1, encoding an essential mitochondrion-targeted prolyl-tRNA synthetase, reveals mitochondrion-dependent down-regulation of photosynthesis. Paolo Pesaresi^*,1, Dario Leister¹, ¹ Max-Planck-Institute for Plant Breeding Research, Koeln, Germany

ABSTRACT- The Arabidopsis prors1-1 and -2 mutants were identified on the basis of a decreased effective quantum yield of photosystem II. The mutations responsible were localized to ProrRS1, encoding the mitochondrial prolyl-tRNA synthethase ProRS1. In atprors1-1 and -2, ProRS1 expression is reduced, resulting into decreased abundance of the mitochondrial respiratory chain. Null alleles of atProRS1, identified by reverse genetics, are affected in ovule development and show an arrest in embryo development at pre-globular stages. The leaky prors1 alleles were used to study mitochondrion-dependent regulation of photosynthesis: in prors1-1 and -2, the expression of nuclear-encoded photosynthetic proteins is down-regulated at the transcriptional level, resulting into a decreased accumulation of all thylakoid multiprotein complexes. Down-regulation of the transcripts persists in the dark, representing an acclimatory response of the chloroplast to adapt the plant cell to the mitochondrial defect. Expression profiling of 3300 nuclear genes was performed for atprors1-1 and -2 and other conditions known to modify the photosynthetic performance. High-light stress and the atprors1-1 and -2 mutations result into similar nuclear transcriptome responses, characterized by a predominant up-regulation of most of the genes analysed and a specific down-regulation of photosynthetic genes. We suggest that the signaling which results into this type of transcriptional down-regulation involves reactive oxygen species, originating from chloroplasts and/or mitochondria.

KEY WORDS: Photosynthesis, Reactive oxygen species, Gene expression regulation, Mitochondria