scholarly journals Subcellular Energetics and Carbon Storage in Chlamydomonas

Cells ◽  
2019 ◽  
Vol 8 (10) ◽  
pp. 1154 ◽  
Author(s):  
Burlacot ◽  
Peltier ◽  
Li-Beisson
Keyword(s):  
Energy Management ◽  
Electron Flow ◽  
Building Blocks ◽  
Acid Synthesis ◽  
Cellular Mechanisms ◽  
Algal Biotechnology ◽  
Atp Production ◽  
Holistic Understanding ◽  
Algal Photosynthesis ◽  
Biotechnology Sector

Microalgae have emerged as a promising platform for production of carbon- and energy- rich molecules, notably starch and oil. Establishing an economically viable algal biotechnology sector requires a holistic understanding of algal photosynthesis, physiology, cell cycle and metabolism. Starch/oil productivity is a combined effect of their cellular content and cell division activities. Cell growth, starch and fatty acid synthesis all require carbon building blocks and a source of energy in the form of ATP and NADPH, but with a different requirement in ATP/NADPH ratio. Thus, several cellular mechanisms have been developed by microalgae to balance ATP and NADPH supply which are essentially produced by photosynthesis. Major energy management mechanisms include ATP production by the chloroplast-based cyclic electron flow and NADPH removal by water-water cycles. Furthermore, energetic coupling between chloroplast and other cellular compartments, mitochondria and peroxisome, is increasingly recognized as an important process involved in the chloroplast redox poise. Emerging literature suggests that alterations of energy management pathways affect not only cell fitness and survival, but also influence biomass content and composition. These emerging discoveries are important steps towards diverting algal photosynthetic energy to useful products for biotechnological applications.

scholarly journals ATP compartmentation in plastids and cytosol ofArabidopsis thalianarevealed by fluorescent protein sensing

2018 ◽  
Vol 115 (45) ◽  
pp. E10778-E10787 ◽  
Author(s):  
Chia Pao Voon ◽  
Xiaoqian Guan ◽  
Yuzhe Sun ◽  
Abira Sahu ◽  
May Ngor Chan ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Fluorescent Protein ◽  
Higher Plants ◽  
Electron Flow ◽  
Cyclic Electron Flow ◽  
Linear Electron ◽  
Protein Sensing ◽  
Atp Production ◽  
Respiratory Inhibitors ◽  
Sensor Protein

Matching ATP:NADPH provision and consumption in the chloroplast is a prerequisite for efficient photosynthesis. In terms of ATP:NADPH ratio, the amount of ATP generated from the linear electron flow does not meet the demand of the Calvin–Benson–Bassham (CBB) cycle. Several different mechanisms to increase ATP availability have evolved, including cyclic electron flow in higher plants and the direct import of mitochondrial-derived ATP in diatoms. By imaging a fluorescent ATP sensor protein expressed in livingArabidopsis thalianaseedlings, we found that MgATP2−concentrations were lower in the stroma of mature chloroplasts than in the cytosol, and exogenous ATP was able to enter chloroplasts isolated from 4- and 5-day-old seedlings, but not chloroplasts isolated from 10- or 20-day-old photosynthetic tissues. This observation is in line with the previous finding that the expression of chloroplast nucleotide transporters (NTTs) inArabidopsismesophyll is limited to very young seedlings. Employing a combination of photosynthetic and respiratory inhibitors with compartment-specific imaging of ATP, we corroborate the dependency of stromal ATP production on mitochondrial dissipation of photosynthetic reductant. Our data suggest that, during illumination, the provision and consumption of ATP:NADPH in chloroplasts can be balanced by exporting excess reductants rather than importing ATP from the cytosol.

scholarly journals Rapid approach to complex boronic acids

2019 ◽  
Vol 5 (7) ◽  
pp. eaaw4607 ◽  
Author(s):  
Constantinos G. Neochoritis ◽  
Shabnam Shaabani ◽  
Maryam Ahmadianmoghaddam ◽  
Tryfon Zarganes-Tzitzikas ◽  
Li Gao ◽  
...  
Keyword(s):  
Small Molecules ◽  
Boronic Acid ◽  
Multicomponent Reactions ◽  
Chemical Space ◽  
Building Blocks ◽  
Acid Synthesis ◽  
Success Rates ◽  
Boronic Acid Derivatives ◽  
Low Coverage ◽  
Target Synthesis

The compatibility of free boronic acid building blocks in multicomponent reactions to readily create large libraries of diverse and complex small molecules was investigated. Traditionally, boronic acid synthesis is sequential, synthetically demanding, and time-consuming, which leads to high target synthesis times and low coverage of the boronic acid chemical space. We have performed the synthesis of large libraries of boronic acid derivatives based on multiple chemistries and building blocks using acoustic dispensing technology. The synthesis was performed on a nanomole scale with high synthesis success rates. The discovery of a protease inhibitor underscores the usefulness of the approach. Our acoustic dispensing–enabled chemistry paves the way to highly accelerated synthesis and miniaturized reaction scouting, allowing access to unprecedented boronic acid libraries.

Photosystem I-abhängige Phosphorylierung isolierter Chloroplasten mit Ascorbat/2.6-Dichlorphenolindophenol als Elektronendonator und Methylviologen als Elektronenakzeptor / Photosystem I Dependent Phosphorylation of Isolated Chloroplasts with Ascorbate/2,6-Dichlorophenolindophenol as Electron Donor and Methylviologen as Electron Acceptor

1972 ◽  
Vol 27 (4) ◽  
pp. 445-455 ◽  
Author(s):  
Heinrich Strotmann ◽  
Christa Von Gösseln
Keyword(s):  
Electron Transport ◽  
Linear System ◽  
Photosystem I ◽  
Electron Acceptor ◽  
Electron Flow ◽  
Phosphorylation Site ◽  
Cyclic System ◽  
Atp Production ◽  
Proton Uptake ◽  
Isolated Chloroplasts

Photosystem I related phosphorylation of isolated chloroplasts was investigated with special reference to the stoichiometry between ATP production and electron transprt (ATP: 2e⊖). The system studied contained DCMU to inhibit electron flow from photosystem II, ascorbate and DPIP to supply electrons to photosystem I, and methylviologen as electron acceptor. The following results were obtained:1. Basal electron transport is stimulated by the addition of the phosphorylating system, indicating that phosphorylation is really coupled to non-cyclic electron flow. The ratio ATP: 2e⊖ is 1, when the increase of electron flow obtained by the addition of ADP and phosphate is correlated to phosphorylation. This ratio is constant upon varying several parameters including DPIP concentration and light intensity.2. In the absence of methylviologen a DPIP catalyzed cyclic phosphorylation takes place (cf. I. c.7, 11, 12). Phosphorylation is not increased by the addition of methylviologen, indicating that both, the cyclic DPIP mediated and the non-cyclic system are coupled to the same phosphorylation site and limited by the same reaction step.3. In the absence of oxygen a methylviologen supported cyclic phosphorylation occurs. Comparing optimum rates, phosphorylation under these conditions is about twice as high as in the noncyclic system. Therefore we conclude that two phosphorylation sites are involved in methylviologen catalyzed cyclic electron transport. This system is sensitive against trypsin treatment of the chloroplasts, whereas the linear system is not.4. The two cyclic systems as well as the non-cyclic system are coupled to reversible proton uptake. Furthermore the linear system exhibits an irreversible uptake of hydrogen ions, which is stoichiometric to electron flow. From the reversible and the irreversible components of the pH changes the ratio of the proton pump to electron transprt can be calculated. Under steady state conditions the ration H⨁ : e⊖ approaches 1.

scholarly journals Autophagy in unicellular eukaryotes

2010 ◽  
Vol 365 (1541) ◽  
pp. 819-830 ◽  
Author(s):  
Jan A. K. W. Kiel
Keyword(s):  
Molecular Mechanisms ◽  
Yeast Species ◽  
Developmental Change ◽  
Building Blocks ◽  
Extracellular Medium ◽  
New Host ◽  
Growth And Survival ◽  
Atp Production ◽  
Unicellular Eukaryotes

Cells need a constant supply of precursors to enable the production of macromolecules to sustain growth and survival. Unlike metazoans, unicellular eukaryotes depend exclusively on the extracellular medium for this supply. When environmental nutrients become depleted, existing cytoplasmic components will be catabolized by (macro)autophagy in order to re-use building blocks and to support ATP production. In many cases, autophagy takes care of cellular housekeeping to sustain cellular viability. Autophagy encompasses a multitude of related and often highly specific processes that are implicated in both biogenetic and catabolic processes. Recent data indicate that in some unicellular eukaryotes that undergo profound differentiation during their life cycle (e.g. kinetoplastid parasites and amoebes), autophagy is essential for the developmental change that allows the cell to adapt to a new host or form spores. This review summarizes the knowledge on the molecular mechanisms of autophagy as well as the cytoplasm-to-vacuole-targeting pathway, pexophagy, mitophagy, ER-phagy, ribophagy and piecemeal microautophagy of the nucleus, all highly selective forms of autophagy that have first been uncovered in yeast species. Additionally, a detailed analysis will be presented on the state of knowledge on autophagy in non-yeast unicellular eukaryotes with emphasis on the role of this process in differentiation.

scholarly journals PKM2, a Central Point of Regulation in Cancer Metabolism

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Nicholas Wong ◽  
Jason De Melo ◽  
Damu Tang
Keyword(s):  
Protein Tyrosine Kinase ◽  
Cancer Metabolism ◽  
Kinase Activity ◽  
Aerobic Glycolysis ◽  
Active Form ◽  
Building Blocks ◽  
Atp Production ◽  
Complex Regulation ◽  
Rate Limiting ◽  
Glucose Metabolites

Aerobic glycolysis is the dominant metabolic pathway utilized by cancer cells, owing to its ability to divert glucose metabolites from ATP production towards the synthesis of cellular building blocks (nucleotides, amino acids, and lipids) to meet the demands of proliferation. The M2 isoform of pyruvate kinase (PKM2) catalyzes the final and also a rate-limiting reaction in the glycolytic pathway. In the PK family, PKM2 is subjected to a complex regulation by both oncogenes and tumour suppressors, which allows for a fine-tone regulation of PKM2 activity. The less active form of PKM2 drives glucose through the route of aerobic glycolysis, while active PKM2 directs glucose towards oxidative metabolism. Additionally, PKM2 possesses protein tyrosine kinase activity and plays a role in modulating gene expression and thereby contributing to tumorigenesis. We will discuss our current understanding of PKM2's regulation and its many contributions to tumorigenesis.

scholarly journals Mitochondrial KATP channels stabilize intracellular Ca2+ during hypoxia in retinal horizontal cells of goldfish (Carassius auratus)

2021 ◽  
Author(s):  
Michael W. Country ◽  
Michael G. Jonz
Keyword(s):  
Carassius Auratus ◽  
Katp Channels ◽  
Horizontal Cells ◽  
Hypoxia Tolerance ◽  
Dependent Manner ◽  
Cellular Mechanisms ◽  
Atp Production ◽  
Goldfish Carassius Auratus ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Mitochondrial Katp Channels

Neurons of the retina require oxygen to survive. In hypoxia, neuronal ATP production is impaired, ATP-dependent ion pumping is reduced, transmembrane ion gradients are dysregulated, and [Ca2+]i increases enough to trigger excitotoxic cell death. Central neurons of the common goldfish (Carassius auratus) are hypoxia-tolerant, but little is known about how goldfish retinas withstand hypoxia. To study the cellular mechanisms of hypoxia tolerance, we isolated retinal interneurons (horizontal cells; HCs), and measured intracellular Ca2+ concentration ([Ca2+]i) with Fura-2. Goldfish HCs maintained [Ca2+]i throughout 1 h of hypoxia, whereas [Ca2+]i increased irreversibly in HCs of the hypoxia-sensitive rainbow trout (Oncorhynchus mykiss) with just 20 min of hypoxia. Our results suggest mitochondrial ATP-dependent K+ channels (mKATP) are necessary to stabilize [Ca2+]i throughout hypoxia. In goldfish HCs, [Ca2+]i increased when mKATP was blocked with glibenclamide or 5-HD, whereas an mKATP agonist (diazoxide) prevented [Ca2+]i from increasing in hypoxia in trout HCs. We showed that hypoxia protects goldfish HCs via mKATP channels. Glycolytic inhibition with 2-deoxyglucose increased [Ca2+]i, which was rescued by hypoxia in an mKATP-dependent manner. We found no evidence of plasmalemmal KATP channels in patch-clamp experiments. Instead, we confirmed the involvement of KATP in mitochondria with TMRE imaging, as hypoxia rapidly (<5 min) depolarized mitochondria in an mKATP-sensitive manner. We conclude that mKATP channels initiate a neuroprotective pathway in goldfish HCs to maintain [Ca2+]i and avoid excitotoxicity in hypoxia. This model provides novel insight into the cellular mechanisms of hypoxia tolerance in the retina.

scholarly journals Impairment of mitochondrial respiratory function as an early biomarker of apoptosis induced by growth factor removal

2017 ◽  
Author(s):  
Hélène Lemieux ◽  
Patrick Subarsky ◽  
Christine Doblander ◽  
Martin Wurm ◽  
Jakob Troppmair ◽  
...  
Keyword(s):  
Intracellular Signaling ◽  
Energy Homeostasis ◽  
Tricarboxylic Acid Cycle ◽  
Electron Flow ◽  
Control Cell ◽  
Building Blocks ◽  
Mitochondrial Outer Membrane ◽  
Early Event ◽  
Complex Iv ◽  
Mitochondrial Energy Metabolism

AbstractIntracellular signaling pathways not only control cell proliferation and survival, but also regulate the provision of cellular energy and building blocks through mitochondrial and non-mitochondrial metabolism. Wild-type and oncogenic RAF kinases have been shown to prevent apoptosis following the removal of interleukin 3 (IL-3) from mouse pro-myeloid 32D cells by reducing mitochondrial reactive oxygen species production. To study primary effects of RAF on mitochondrial energy metabolism, we applied high-resolution respirometry after short-term IL-3 deprivation (8 h), before 32D cells show detectable signs of cell death. Respiration in intact 32D cells was suppressed as an early event following removal of IL-3, but remained more stable in 32D cells expressing the v-RAF oncogene. In permeabilized 32D cells deprived of IL-3, respiratory capacities of the NADH-pathway, the convergent NADH&succinate-pathway, and Complex IV activity were decreased compared to cells grown in the presence of IL-3, whereas succinate-supported respiration remained unchanged, consistent with control by Complex IV. The apparent Complex IV excess capacity was zero above NADH&succinate-pathway capacity reconstituting tricarboxylic acid cycle function. In comparison, electron flow reached only 60% when supported by succinate alone through Complexes II, III and IV, and was therefore relatively insensitive to Complex IV injuries up to a threshold of 40% inhibition. A slight increase in respiration following addition of cytochrome c, a marker of mitochondrial outer membrane leakage, was present after IL-3 depletion, indicating mitochondrial fragility. Our results highlight a novel link between the key mitogenic and survival kinase CRAF and mitochondrial energy homeostasis.

scholarly journals The Role of Mitonuclear Incompatibility in Bipolar Disorder Susceptibility and Resilience Against Environmental Stressors

2021 ◽  
Vol 12 ◽  
Author(s):  
Suzanne Gonzalez
Keyword(s):  
Bipolar Disorder ◽  
Oxidative Phosphorylation ◽  
Mitochondrial Dysfunction ◽  
Brain Function ◽  
Electron Flow ◽  
Mitochondrial Genes ◽  
Environmental Stressors ◽  
Atp Production ◽  
Co Morbidity

It has been postulated that mitochondrial dysfunction has a significant role in the underlying pathophysiology of bipolar disorder (BD). Mitochondrial functioning plays an important role in regulating synaptic transmission, brain function, and cognition. Neuronal activity is energy dependent and neurons are particularly sensitive to changes in bioenergetic fluctuations, suggesting that mitochondria regulate fundamental aspects of brain function. Vigorous evidence supports the role of mitochondrial dysfunction in the etiology of BD, including dysregulated oxidative phosphorylation, general decrease of energy, altered brain bioenergetics, co-morbidity with mitochondrial disorders, and association with genetic variants in mitochondrial DNA (mtDNA) or nuclear-encoded mitochondrial genes. Despite these advances, the underlying etiology of mitochondrial dysfunction in BD is unclear. A plausible evolutionary explanation is that mitochondrial-nuclear (mitonuclear) incompatibility leads to a desynchronization of machinery required for efficient electron transport and cellular energy production. Approximately 1,200 genes, encoded from both nuclear and mitochondrial genomes, are essential for mitochondrial function. Studies suggest that mitochondrial and nuclear genomes co-evolve, and the coordinated expression of these interacting gene products are essential for optimal organism function. Incompatibilities between mtDNA and nuclear-encoded mitochondrial genes results in inefficiency in electron flow down the respiratory chain, differential oxidative phosphorylation efficiency, increased release of free radicals, altered intracellular Ca2+ signaling, and reduction of catalytic sites and ATP production. This review explores the role of mitonuclear incompatibility in BD susceptibility and resilience against environmental stressors.

scholarly journals Characteristics of Neural Network Changes in Normal Aging and Early Dementia

2021 ◽  
Vol 13 ◽  
Author(s):  
Hirohisa Watanabe ◽  
Epifanio Bagarinao ◽  
Satoshi Maesawa ◽  
Kazuhiro Hara ◽  
Kazuya Kawabata ◽  
...  
Keyword(s):  
Multisensory Integration ◽  
Resting State ◽  
Energy Supply ◽  
Healthy Aging ◽  
Supply And Demand ◽  
Cellular Level ◽  
Functional Network ◽  
Cellular Mechanisms ◽  
Atp Production ◽  
The Brain

To understand the mechanisms underlying preserved and impaired cognitive function in healthy aging and dementia, respectively, the spatial relationships of brain networks and mechanisms of their resilience should be understood. The hub regions of the brain, such as the multisensory integration and default mode networks, are critical for within- and between-network communication, remain well-preserved during aging, and play an essential role in compensatory processes. On the other hand, these brain hubs are the preferred sites for lesions in neurodegenerative dementias, such as Alzheimer’s disease. Disrupted primary information processing networks, such as the auditory, visual, and sensorimotor networks, may lead to overactivity of the multisensory integration networks and accumulation of pathological proteins that cause dementia. At the cellular level, the brain hub regions contain many synapses and require a large amount of energy. These regions are rich in ATP-related gene expression and had high glucose metabolism as demonstrated on positron emission tomography (PET). Importantly, the number and function of mitochondria, which are the center of ATP production, decline by about 8% every 10 years. Dementia patients often have dysfunction of the ubiquitin-proteasome and autophagy-lysosome systems, which require large amounts of ATP. If there is low energy supply but the demand is high, the risk of disease can be high. Imbalance between energy supply and demand may cause accumulation of pathological proteins and play an important role in the development of dementia. This energy imbalance may explain why brain hub regions are vulnerable to damage in different dementias. Here, we review (1) the characteristics of gray matter network, white matter network, and resting state functional network changes related to resilience in healthy aging, (2) the mode of resting state functional network disruption in neurodegenerative dementia, and (3) the cellular mechanisms associated with the disruption.

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