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A mutation in the Arabidopsis mTERF-related plastid protein SOLDAT10 activates retrograde signaling and suppresses <sup>1</sup>O<sub>2</sub>-induced cell death
Auteur(s)
Meskauskiene, Rasa
Würsch, Marco
Laloi, Christophe
Vidi, Pierre-Alexandre
Coll, Núria S.
Baruah, Aiswarya
Kim, Chanhong
Apel, Klaus
Date de parution
2009
In
The Plant Journal, Wiley, 2009/60/3/399-410
Résumé
The conditional <i>flu</i> mutant of <i>Arabidopsis thaliana</i> generates singlet oxygen (<sup>1</sup>O<sub>2</sub>) in plastids during a dark-to-light shift. Seedlings of <i>flu</i> bleach and die, whereas mature plants stop growing and develop macroscopic necrotic lesions. Several suppressor mutants, dubbed singlet oxygen-linked death activator (<i>soldat</i>), were identified that abrogate <sup>1</sup>O<sub>2</sub>-mediated cell death of <i>flu</i> seedlings. One of the soldat mutations, <i>soldat10</i>, affects a gene encoding a plastid-localized protein related to the human mitochondrial transcription termination factor mTERF. As a consequence of this mutation, plastid-specific rRNA levels decrease and protein synthesis in plastids of <i>soldat10</i> is attenuated. This disruption of chloroplast homeostasis in <i>soldat10</i> seedlings affects communication between chloroplasts and the nucleus and leads to changes in the steady-state concentration of nuclear gene transcripts. The <i>soldat10</i> seedlings suffer from mild photo-oxidative stress, as indicated by the constitutive up-regulation of stress-related genes. Even though <i>soldat10/flu</i> seedlings overaccumulate the photosensitizer protochlorophyllide in the dark and activate the expression of <sup>1</sup>O<sub>2</sub>-responsive genes after a dark-to-light shift they do not show a <sup>1</sup>O<sub>2</sub>-dependent cell death response. Disturbance of chloroplast homeostasis in emerging <i>soldat10/flu</i> seedlings seems to antagonize a subsequent <sup>1</sup>O<sub>2</sub>-mediated cell death response without suppressing <sup>1</sup>O<sub>2</sub>-dependent retrograde signaling. The results of this work reveal the unexpected complexity of what is commonly referred to as 'plastid signaling'.
Identifiants
Type de publication
journal article
