scholarly journals Nutrient gradients simulate different adjustments of coral-algal symbiosis

2020 ◽  
Author(s):  
Haoya Tong ◽  
Guowei Zhou ◽  
Fang Zhang ◽  
Jin Sun ◽  
Weipeng Zhang ◽  
...  
Keyword(s):  
Nitrogen Metabolism ◽  
Atp Synthesis ◽  
Pocillopora Damicornis ◽  
Material Transport ◽  
Coral Larvae ◽  
Coral Larva ◽  
Algal Symbiosis ◽  
Energy Synthesis ◽  
Coral Reef Degradation ◽  
Transcriptomic Responses

Abstract Background: Eutrophication is one of the major causes of coral reef degradation but the effect of eutrophication on coral and its symbiont algae remains unclear, particularly for the larval stage of coral. In the present study, the physiological and transcriptomic responses of the larvae of an ecologically important scleractinian coral Pocillopora damicornis were analyzed after a 5-day exposure to elevated nitrate in order to assess the survival and adaptation of coral-algal symbiosis under elevated nutrients. Results: The results showed that multiple larval transcripts were significantly correlated with Symbiodiniaceae transcripts. The major differentially expressed transcripts in coral/Symbiodiniaceae included those responsible for energy synthesis/comsumption, nitrogen metabolism and stressor response. Slightly elevated nitrate concentration could in fact promote the health of coral meta-organism. With increase in nitrate concentrations, coral larvae showed significant stress response to maintain the coral-algal symbiosis and coral-algal symbiosis was impaired, while Symbiodiniaceae switched photosynthetic states for ATP synthesis, material transport and nitrogen metabolism for symbiosis maintenance under the control of the coral hosts.Conclusions: Our results suggest that adjustment of coral-algal symbiosis via coral control and a shift in Symbiodiniaceae photosynthetic states serves as the basis of coral meta-organism adaptation under eutrophication stresses. The larvae of P. damicornis and Symbiodiniaceae displayed different transcriptomic responses to nitrate enrichment. Coral larva meta-organism can adapt to moderately elevated nutrient concentration while extreme eutrophication can impair coral-algal symbiosis and affect coral larvae survival ultimately.

Limited transfer of cytosolic NADH into mitochondria at high cardiac workload

2004 ◽  
Vol 286 (6) ◽  
pp. H2237-H2242 ◽  
Author(s):  
J. Michael O'Donnell ◽  
Raymond K. Kudej ◽  
Kathyrn F. LaNoue ◽  
Stephen F. Vatner ◽  
E. Douglas Lewandowski
Keyword(s):  
Blood Flow ◽  
Glucose Oxidation ◽  
Lactate Production ◽  
Atp Synthesis ◽  
Rate Pressure Product ◽  
Myocardial Tissue ◽  
High Workload ◽  
Energy Synthesis ◽  
High Work ◽  
Reducing Equivalents

Glycolysis supplements energy synthesis at high cardiac workloads, producing not only ATP but also cytosolic NADH and pyruvate for oxidative ATP synthesis. Despite adequate Po2, speculation exists that not all cytosolic NADH is oxidized by the mitochondria, leading to lactate production. In this study, we elucidate the mechanism for limited cytosolic NADH oxidation and increased lactate production at high workload despite adequate myocardial blood flow and oxygenation. Reducing equivalents from glycolysis enter mitochondria via exchange of mitochondrial α-ketoglutarate (α-KG) for cytosolic malate. This exchange was monitored at baseline and at high workloads by comparing 13C enrichment between the products of α-KG oxidation (succinate) and α-KG efflux from mitochondria (glutamate). Under general anesthesia, a left thoracotomy was performed on 14 dogs and [2-13C]acetate was infused into the left anterior descending artery for 40 min. The rate-pressure product was 9,035 ± 1,972 and 21,659 ± 5,266 mmHg·beats·min−1 ( n = 7) at baseline ( n = 7) and with dobutamine, respectively. 13C enrichment of succinate was 57 ± 10% at baseline and 45 ± 13% at elevated workload (not significant), confirming oxidation of [2-13C]acetate. However, cytosolic glutamate enrichment, a marker of cytosolic NADH transfer to mitochondria, was dramatically reduced at high cardiac workload (11 ± 1%) vs. baseline (50 ± 14%, P < 0.05). This reduced exchange of 13C from α-KG to cytosolic glutamate at high work indicates reduced shuttling of cytosolic reducing equivalents into the mitochondria. Myocardial tissue lactate increased 78%, countering this reduced oxidation of cytosolic NADH. The findings elucidate a contributing mechanism to glycolysis outpacing glucose oxidation in the absence of myocardial ischemia.

scholarly journals Microinjection to deliver protein, mRNA, and DNA into zygotes of the cnidarian endosymbiosis model Aiptasia sp.

2017 ◽  
Author(s):  
Victor A. S. Jones ◽  
Madeline Bucher ◽  
Elizabeth A. Hambleton ◽  
Annika Guse
Keyword(s):  
Transgene Expression ◽  
Molecular Mechanisms ◽  
Model System ◽  
Proof Of Concept ◽  
Coral Larvae ◽  
Functional Studies ◽  
Algal Symbiosis ◽  
Summary Statement ◽  
Exogenous Genes

AbstractReef-building corals depend on an intracellular symbiosis with photosynthetic dinoflagellates for their survival in nutrient-poor oceans. Symbionts are phagocytosed by coral larvae from the environment and transfer essential nutrients to their hosts. Aiptasia, a small tropical marine sea anemone, is emerging as a tractable model system for coral symbiosis; however, to date functional tools and genetic transformation are lacking. Here we have established an efficient workflow to collect Aiptasia eggs for in vitro fertilization and microinjection as the basis for experimental manipulations in the developing embryo and larvae. We demonstrate that protein, mRNA, and DNA can successfully be injected into live Aiptasia zygotes to label actin with recombinant Lifeact-eGFP protein; to label nuclei and cell membranes with NLS-eGFP and farnesylated mCherry translated from injected mRNA; and to transiently drive transgene expression from an Aiptasia-specific promoter, respectively, in embryos and larvae. These proof-of-concept approaches pave the way for future functional studies of development and symbiosis establishment in Aiptasia, a powerful model to unravel the molecular mechanisms underlying intracellular coral-algal symbiosis.Summary StatementToolkit extension: development of microinjection for cellular labelling, expression of exogenous genes and live imaging in Aiptasia, an emerging model for intracellular coral-algal symbiosis.

scholarly journals The mitochondrial calcium uniporter compensates for Complex I dysfunction

2021 ◽  
Author(s):  
Enrique Balderas ◽  
David Eberhardt ◽  
John Pleinis ◽  
Salah Sommakia ◽  
Anthony Balynas ◽  
...  
Keyword(s):  
Protein Turnover ◽  
Complex I ◽  
Atp Synthesis ◽  
Signaling Mechanism ◽  
Mitochondrial Calcium Uniporter ◽  
Calcium Uniporter ◽  
Complex I Deficiency ◽  
Transport Chain ◽  
Energy Synthesis ◽  
And Function

Abstract Calcium (Ca2+) entering mitochondria potently stimulates ATP synthesis. Increases in Ca2+ preserve energy synthesis in cardiomyopathies caused by mitochondrial dysfunction, and occur due to enhanced activity of the mitochondrial Ca2+ uniporter channel. The signaling mechanism that mediates this compensatory increase remains unknown. Here, we find that increases in the uniporter are due to impairment in Complex I of the electron transport chain (ETC). In normal physiology, Complex I promotes uniporter degradation via an interaction with the uniporter pore-forming subunit, a process we term Complex I-induced protein turnover (CLIPT). When Complex I dysfunction ensues, contact with the uniporter is inhibited, preventing degradation, and leading to a build-up in functional channels. Preventing uniporter activity leads to early demise in Complex I-deficient animals. Conversely, enhancing uniporter stability rescues survival and function in Complex I deficiency. Taken together, our data identify a fundamental pathway producing compensatory increases in Ca2+ influx during Complex I impairment.

scholarly journals Varied effects of algal symbionts on transcription factor NF-κB in a sea anemone and a coral: possible roles in symbiosis and thermotolerance

2019 ◽  
Author(s):  
Katelyn M. Mansfield ◽  
Phillip A. Cleves ◽  
Emily Van Vlack ◽  
Nicola G. Kriefall ◽  
Brooke E. Benson ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Target Genes ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Pocillopora Damicornis ◽  
Coral Colony ◽  
Algal Symbionts ◽  
Genome Wide ◽  
Algal Symbiosis ◽  
Clade C

AbstractMany cnidarians, including the reef-building corals, undergo symbiotic mutualisms with photosynthetic dinoflagellate algae of the family Symbiodiniaceae. These partnerships are sensitive to temperature extremes, which cause symbiont loss and increased coral mortality. Previous studies have implicated host immunity and specifically immunity transcription factor NF-κB as having a role in the maintenance of the cnidarian-algal symbiosis. Here we have further investigated a possible role for NF-κB in establishment and loss of symbiosis in various strains of the anemone Exaiptasia (Aiptasia) and in the coral Pocillopora damicornis. Our results show that NF-κB expression is reduced in Aiptasia larvae and adults that host certain algae strains. Treatment of Aiptasia larvae with a known symbiosis-promoting cytokine, transforming growth factor β, also led to decreased NF-κB expression. We also show that aposymbiotic Aiptasia (with high NF-κB expression) have increased survival following infection with the pathogenic bacterium Serratia marcescens as compared to symbiotic Aiptasia (low NF-κB expression). Furthermore, a P. damicornis coral colony hosting Durusdinium spp. (formerly clade D) symbionts had higher basal NF-κB expression and decreased heat-induced bleaching as compared to two individuals hosting Cladocopium spp. (formerly clade C) symbionts. Lastly, genome-wide gene expression profiling and genomic promoter analysis identified putative NF-κB target genes that may be involved in thermal bleaching, symbiont maintenance, and/or immune protection in P. damicornis. Our results provide further support for the hypothesis that modulation of NF-κB and immunity plays a role in some, but perhaps not all, cnidarian-Symbiodiniaceae partnerships as well as in resistance to pathogens and bleaching.

Effects of Neuroactive Amino Acids Derivatives on Cardiac and Cerebral Mitochondria and Endothelial functions in Animals Exposed to Stress

2017 ◽  
Vol 2 (2) ◽  
pp. 34
Author(s):  
TA Popova ◽  
II Prokofiev ◽  
IS Mokrousov ◽  
Valentina Perfilova ◽  
AV Borisov ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Platelet Aggregation ◽  
Atp Synthesis ◽  
Elevated Concentration ◽  
Blood Pressure Monitor ◽  
Pressure Monitor ◽  
Griess Reagent ◽  
Arterial Blood ◽  
Endothelial Functions

Introduction: To study the effects of glufimet, a new derivative of glutamic acid, and phenibut, a derivative of γ-aminobutyric acid (GABA), on cardiac and cerebral mitochondria and endothelial functions in animals following exposure to stress and inducible nitric oxide synthase (iNOS) inhibition. Methods: Rats suspended by their dorsal cervical skin fold for 24 hours served as the immobilization and pain stress model. Arterial blood pressure was determined using a non-invasive blood pressure monitor. Mitochondrial fraction of heart and brain homogenates were isolated by differential centrifugation and analysed for mitochondrial respiration intensity, lipid peroxidation (LPO) and antioxidant enzyme activity using polarographic method. The concentrations of nitric oxide (NO) terminal metabolites were measured using Griess reagent. Hemostasis indices were evaluated. Platelet aggregation was estimated using modified version of the Born method described by Gabbasov et al., 1989. Results: The present study demonstrated that stress leads to an elevated concentration of NO terminal metabolites and LPO products, decreased activity of antioxidant enzymes, reduced mitochondrial respiratory function, and endothelial dysfunction. Inhibition of iNOS by aminoguanidine had a protective effect. Phenibut and glufimet inhibited a rise in stress-induced nitric oxide production. This resulted in enhanced coupling of substrate peroxidation and ATP synthesis. The reduced LPO processes caused by glufimet and phenibut normalized the endothelial function which was proved by the absence of average daily blood pressure (BP) elevation episodes and a significant increase in platelet aggregation level. Conclusion: Glufimet and phenibut restrict the harmful effects of stress on the heart and brain possibly by modulating iNOS activity.

Diethylstilbestrol and Length of Preliminary Period in the Utilization of Crude Biuret and Urea by Lambs. II. Various Aspects of Nitrogen Metabolism

1960 ◽  
Vol 19 (1) ◽  
pp. 44-53 ◽  
Author(s):  
G. A. McLaren ◽  
G. C. Anderson ◽  
J. A. Welch ◽  
C. D. Campbell ◽  
G. S. Smith
Keyword(s):  
Nitrogen Metabolism
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