A mutation in the Arabidopsis mTERF-related plastid protein SOLDAT10 activates retrograde signaling and suppresses ¹O₂-induced cell death

The conditional <i>flu</i> mutant of <i>Arabidopsis thaliana</i> generates singlet oxygen (¹O₂) 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 ¹O₂-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 ¹O₂-responsive genes after a dark-to-light shift they do not show a ¹O₂-dependent cell death response. Disturbance of chloroplast homeostasis in emerging <i>soldat10/flu</i> seedlings seems to antagonize a subsequent ¹O₂-mediated cell death response without suppressing ¹O₂-dependent retrograde signaling. The results of this work reveal the unexpected complexity of what is commonly referred to as 'plastid signaling'.