scholarly journals Plastid gene expression is required for singlet oxygen-induced chloroplast degradation and cell death

2020 ◽  
Author(s):  
Kamran Alamdari ◽  
Karen E. Fisher ◽  
Andrew B. Sinson ◽  
Joanne Chory ◽  
Jesse D. Woodson
Keyword(s):  
Gene Expression ◽  
Reactive Oxygen Species ◽  
Cell Death ◽  
Singlet Oxygen ◽  
Chloroplast Development ◽  
Nuclear Gene ◽  
Oxygen Species ◽  
Plastid Gene ◽  
Plastid Gene Expression ◽  
Nuclear Gene Expression

SummaryChloroplasts constantly experience photo-oxidative stress while performing photosynthesis. This is particularly true under abiotic stresses that lead to the accumulation of reactive oxygen species (ROS). While ROS leads to the oxidation of DNA, proteins, and lipids, it can also act as a signal to induce acclimation through chloroplast degradation, cell death, and nuclear gene expression. Although the mechanisms behind ROS signaling from chloroplasts remain mostly unknown, several genetic systems have been devised in the model plant Arabidopsis to understand their signaling properties. One system uses the plastid ferrochelatase two (fc2) mutant that conditionally accumulates the ROS singlet oxygen (1O2) leading to chloroplast degradation and eventually cell death. Here we have mapped three mutations that suppress chloroplast degradation in the fc2 mutant and demonstrate that they affect two independent loci (PPR30 and mTERF9) encoding chloroplast proteins predicted to be involved in post-transcriptional gene expression. Mutations in either gene were shown to lead to broadly reduced chloroplast gene expression, impaired chloroplast development, and reduced chloroplast stress signaling. In these mutants, however, 1O2 levels were uncoupled to chloroplast degradation suggesting that PPR30 and mTERF9 are involved in ROS signaling pathways. In the wild type background, ppr30 and mTERF9 mutants were also observed to be less susceptible to cell death induced by excess light stress. Together these results suggest that plastid gene expression (or the expression of specific plastid genes) is a necessary prerequisite for chloroplasts to activate 1O2 signaling pathways to induce chloroplast degradation and/or cell death.Significance summaryReactive oxygen species accumulate in the chloroplast (photosynthetic plastids) and signal for stress acclimation by inducing chloroplast degradation, cell death, and changes in nuclear gene expression. We have identified two chloroplast-localized proteins involved in gene regulation that are required to transmit these signals, suggesting that proper plastid gene expression and chloroplast development is necessary to activate chloroplast controlled cellular degradation and nuclear gene expression pathways.

The complexity of gene expression in higher plants

1986 ◽  
Vol 314 (1166) ◽  
pp. 481-492 ◽  
Keyword(s):  
Gene Expression ◽  
Transcriptional Control ◽  
Higher Plants ◽  
Nuclear Gene ◽  
Nuclear Genes ◽  
High Concentration ◽  
Plastid Gene ◽  
Plastid Gene Expression ◽  
Nuclear Gene Expression ◽  
Chloroplast Formation

During light-induced chloroplast formation in higher plants the synthesis of several nuclear encoded plastid proteins is under the control of phytochrome. Light acting through the phytochrome system is able both to increase the transcription of certain nuclear genes and to decrease the transcription of others. It has been generally assumed that regulation by phytochrome alone would be sufficient to account for the observed light-dependent changes in nuclear gene expression during chloroplast formation. However, it has recently become evident that the light-dependent control of nuclear gene expression may be far more complex than originally expected. There are at least two other factors that in addition to phytochrome may affect nuclear gene expression: (1) changes in chromatin organization from an inactive to a transcriptionally active state, and (2) a plastid-derived factor that seems to be involved in the transcriptional control of some nuclear genes encoding plastid-specific proteins. Although the light-dependent control of transcription has been studied intensively for nuclear genes, much less is known about the light-dependent control of plastid gene expression. The P700 chlorophyll a protein of photosystem I is a major membrane protein whose massive accumulation is induced by light and whose genes have been located on the plastid DNA. In barley a high concentration of mRNA for the P700 chlorophyll a protein was detected within the total RNA as well as within the polysomal fraction of etioplasts and remained almost constant during greening. Based on these results it can be inferred that the accumulation of the P700 chlorophyll a protein during light-dependent chloroplast development in barley is not coupled to its transcript concentration but is controlled at a translational — or post-translational - level. The possible function of protochlorophyllide as photoreceptor in this light-dependent control of plastid gene expression is discussed.

scholarly journals Phosphatidylglycerol synthesis facilitates plastid gene expression and light induction of nuclear photosynthetic genes

2021 ◽  
Author(s):  
Sho Fujii ◽  
Koichi Kobayashi ◽  
Ying-Chen Lin ◽  
Yu-chi Liu ◽  
Yuki Nakamura ◽  
...  
Keyword(s):  
Gene Expression ◽  
Chloroplast Development ◽  
Oxygen Species ◽  
Light Conditions ◽  
Plastid Gene ◽  
Plastid Gene Expression ◽  
Plastid Genomes ◽  
Photosynthetic Genes ◽  
Chlorophyll Accumulation ◽  
Arabidopsis Mutant

AbstractPhosphatidylglycerol (PG) is the only major phospholipid in the thylakoid membrane of chloroplasts. PG is essential for photosynthesis and loss of PG in Arabidopsis thaliana results in severe defects of growth and chloroplast development with decreased chlorophyll accumulation, impaired thylakoid formation, and downregulation of photosynthesis-associated genes encoded in nuclear and plastid genomes. However, how the absence of PG affects the gene expression and plant growth remains unclear. To elucidate this mechanism, we investigated the growth and transcriptional profiles of a PG-deficient Arabidopsis mutant pgp1-2 under various light conditions. Microarray analysis demonstrated that reactive oxygen species-responsive genes were upregulated in pgp1-2. Decreased growth light did not alleviated the impaired leaf development and the downregulation of photosynthesis-associated genes in pgp1-2, indicating limited impacts of photooxidative stress on the defects of pgp1-2. Illumination to dark-adapted pgp1-2 triggered downregulation of photosynthesis-associated nuclear-encoded genes (PhANGs), while plastid-encoded genes were constantly suppressed. Overexpression of GOLDEN2-LIKE1 (GLK1), a transcription factor regulating chloroplast development, in pgp1-2 upregulated PhANGs but not plastid-encoded genes along with chlorophyll accumulation. Our data suggest a broad impact of PG biosynthesis on nuclear-encoded genes partially via GLK1 and a specific involvement of this lipid in the plastid gene expression and plant development.

scholarly journals TheArabidopsisSAFEGUARD1 suppresses singlet oxygen-induced stress responses by protecting grana margins

2020 ◽  
Vol 117 (12) ◽  
pp. 6918-6927 ◽  
Author(s):  
Liangsheng Wang ◽  
Dario Leister ◽  
Li Guan ◽  
Yi Zheng ◽  
Katja Schneider ◽  
...  
Keyword(s):  
Singlet Oxygen ◽  
Signaling Pathway ◽  
Stress Responses ◽  
Double Mutant ◽  
Nuclear Gene ◽  
Oxygen Species ◽  
Nuclear Gene Expression ◽  
Induced Stress ◽  
Transcriptional Rewiring ◽  
Chloroplast Stroma

Singlet oxygen (1O2), the major reactive oxygen species (ROS) produced in chloroplasts, has been demonstrated recently to be a highly versatile signal that induces various stress responses. In thefluorescent(flu) mutant, its release causes seedling lethality and inhibits mature plant growth. However, these drastic phenotypes are suppressed when EXECUTER1 (EX1) is absent in theflu ex1double mutant. We identified SAFEGUARD1 (SAFE1) in a screen of ethyl methanesulfonate (EMS) mutagenizedflu ex1plants for suppressor mutants with aflu-like phenotype. Influ ex1 safe1, all1O2-induced responses, including transcriptional rewiring of nuclear gene expression, return to levels, such as, or even higher than, those influ. Without SAFE1, grana margins (GMs) of chloroplast thylakoids (Thys) are specifically damaged upon1O2generation and associate with plastoglobules (PGs). SAFE1 is localized in the chloroplast stroma, and release of1O2induces SAFE1 degradation via chloroplast-originated vesicles. Our paper demonstrates thatflu-produced1O2triggers an EX1-independent signaling pathway and proves that SAFE1 suppresses this signaling pathway by protecting GMs.

Increased efflux of glutathione conjugate in acutely diabetic cardiomyocytes

2004 ◽  
Vol 82 (10) ◽  
pp. 879-887 ◽  
Author(s):  
Sanjoy Ghosh ◽  
Simon Ting ◽  
Howard Lau ◽  
Thomas Pulinilkunnil ◽  
Ding An ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Reactive Oxygen Species ◽  
Cell Death ◽  
Multidrug Resistance ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Multidrug Resistance Protein ◽  
Multidrug Resistance Protein 1 ◽  
Resistance Protein

In diabetes, cell death and resultant cardiomyopathy have been linked to oxidative stress and depletion of antioxidants like glutathione (GSH). Although the de novo synthesis and recycling of GSH have been extensively studied in the chronically diabetic heart, their contribution in modulating cardiac oxidative stress in acute diabetes has been largely ignored. Additionally, the possible contribution of cellular efflux in regulating GSH levels during diabetes is unknown. We used streptozotocin to make Wistar rats acutely diabetic and after 4 days examined the different processes that regulate cardiac GSH. Reduction in myocyte GSH in diabetic rats was accompanied by increased oxidative stress, excessive reactive oxygen species, and an elevated apoptotic cell death. The effect on GSH was not associated with any change in either synthesis or recycling, as both γ-glutamylcysteine synthetase gene expression (responsible for bio syn thesis) and glutathione reductase activity (involved with GSH recycling) remained unchanged. However, gene expression of multidrug resistance protein 1, a transporter implicated in effluxing GSH during oxidative stress, was elevated. GSH conjugate efflux mediated by multidrug resistance protein 1 also increased in diabetic cardiomyocytes, an effect that was blocked using MK-571, a specific inhibitor of this transporter. As MK-571 also decreased oxidative stress in diabetic cardiomyocytes, an important role can be proposed for this transporter in GSH and reactive oxygen species homeostasis in the acutely diabetic heart. Key words: cardiomyocytes, apoptosis, multidrug resistance protein, reactive oxygen species.

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