scholarly journals Manganese Benefits Heat-Stressed Corals at the Cellular Level

2021 ◽  
Vol 8 ◽  
Author(s):  
Enrico Montalbetti ◽  
Tom Biscéré ◽  
Christine Ferrier-Pagès ◽  
Fanny Houlbrèque ◽  
Ivan Orlandi ◽  
...  

The intensity and frequency of coral bleaching events have increased worldwide especially due to thermal stress and seawater pollution. Although it has been observed that metal concentration in seawater can affect the coral’s ability to adopt cellular defensive mechanisms to counteract bleaching, more investigations are needed to better understand the role of metals in coral physiology. In this study, we analyzed the individual and combined effects of prolonged heat stress and manganese (Mn) and iron (Fe) enrichments at the cellular level on the coral Stylophora pistillata. Thermal stress caused an up-regulation in the expression of the host Heat shock proteins (Hsps) 60 and 70, which showed a parallel pattern of modulation in all treatments, as well as an increase of lipid peroxidation (LPO) in the holobiont. Fe enrichment did not induce any change in Hsp expression or in the oxidative status of the corals both at the ambient temperature of 26°C or at increased temperature, suggesting that Fe didn’t seem to play a role in mitigating the cellular damages and the coral bleaching. Mn or MnFe enrichment at 26°C seemed to increase the oxidative stress in zooxanthellae, since high LPO and glutathione reductase (GR) levels were recorded, but it did not cause any effect on polyp Hsp expression, probably due to the antioxidant action of GR. With the temperature increase, Mn enrichments prevented any increase in Hsp levels and caused a significant decrease of LPO and GR activity, strengthening a previous hypothesis suggesting that Mn could mitigate the negative cellular effects produced by the thermal stress.

2021 ◽  
Vol 7 (2) ◽  
pp. eaba9958
Author(s):  
Maxence Guillermic ◽  
Louise P. Cameron ◽  
Ilian De Corte ◽  
Sambuddha Misra ◽  
Jelle Bijma ◽  
...  

The combination of thermal stress and ocean acidification (OA) can more negatively affect coral calcification than an individual stressors, but the mechanism behind this interaction is unknown. We used two independent methods (microelectrode and boron geochemistry) to measure calcifying fluid pH (pHcf) and carbonate chemistry of the corals Pocillopora damicornis and Stylophora pistillata grown under various temperature and pCO2 conditions. Although these approaches demonstrate that they record pHcf over different time scales, they reveal that both species can cope with OA under optimal temperatures (28°C) by elevating pHcf and aragonite saturation state (Ωcf) in support of calcification. At 31°C, neither species elevated these parameters as they did at 28°C and, likewise, could not maintain substantially positive calcification rates under any pH treatment. These results reveal a previously uncharacterized influence of temperature on coral pHcf regulation—the apparent mechanism behind the negative interaction between thermal stress and OA on coral calcification.


2011 ◽  
Vol 22 (19) ◽  
pp. 3571-3583 ◽  
Author(s):  
Toyohide Shinkawa ◽  
Ke Tan ◽  
Mitsuaki Fujimoto ◽  
Naoki Hayashida ◽  
Kaoru Yamamoto ◽  
...  

Heat shock response is characterized by the induction of heat shock proteins (HSPs), which facilitate protein folding, and non-HSP proteins with diverse functions, including protein degradation, and is regulated by heat shock factors (HSFs). HSF1 is a master regulator of HSP expression during heat shock in mammals, as is HSF3 in avians. HSF2 plays roles in development of the brain and reproductive organs. However, the fundamental roles of HSF2 in vertebrate cells have not been identified. Here we find that vertebrate HSF2 is activated during heat shock in the physiological range. HSF2 deficiency reduces threshold for chicken HSF3 or mouse HSF1 activation, resulting in increased HSP expression during mild heat shock. HSF2-null cells are more sensitive to sustained mild heat shock than wild-type cells, associated with the accumulation of ubiquitylated misfolded proteins. Furthermore, loss of HSF2 function increases the accumulation of aggregated polyglutamine protein and shortens the lifespan of R6/2 Huntington's disease mice, partly through αB-crystallin expression. These results identify HSF2 as a major regulator of proteostasis capacity against febrile-range thermal stress and suggest that HSF2 could be a promising therapeutic target for protein-misfolding diseases.


Author(s):  
Karina González ◽  
Juan Gaitán-Espitia ◽  
Alejandro Font ◽  
César A. Cárdenas ◽  
Marcelo González-Aravena

Author(s):  
Scott Hotaling ◽  
Alisha A. Shah ◽  
Kerry L. McGowan ◽  
Lusha M. Tronstad ◽  
J. Joseph Giersch ◽  
...  

AbstractRapid glacier recession is altering the physical conditions of headwater streams. Stream temperatures are predicted to rise and become increasingly variable, putting entire meltwater-associated biological communities at risk of extinction. Thus, there is a pressing need to understand how thermal stress affects mountain stream insects, particularly where glaciers are likely to vanish on contemporary timescales. In this study, we tested the critical thermal maximum (CTMAX) of stonefly nymphs representing multiple species and a range of thermal regimes in the high Rocky Mountains, USA. We then collected RNA-sequencing data to assess how organismal thermal stress translated to the cellular level. Our focal species included the meltwater stonefly, Lednia tumana, which was recently listed under the U.S. Endangered Species Act due to climate-induced habitat loss. For all study species, critical thermal maxima (CTMAX > 20°C) far exceeded the stream temperatures mountain stoneflies experience (< 10°C). Moreover, while evidence for a cellular stress response was present, we also observed constitutive expression of genes encoding proteins known to underlie thermal stress (i.e., heat shock proteins) even at low temperatures that reflected natural conditions. We show that high-elevation aquatic insects may not be physiologically threatened by short-term exposure to warm temperatures and that longer term physiological responses or biotic factors (e.g., competition) may better explain their extreme distributions.


2018 ◽  
Author(s):  
R. J. Murphy ◽  
P. R. Buenzli ◽  
R. E. Baker ◽  
M. J. Simpson

AbstractMechanical heterogeneity in biological tissues, in particular stiffness, can be used to distinguish between healthy and diseased states. However, it is often difficult to explore relationships between cellular-level properties and tissue-level outcomes when biological experiments are performed at a single scale only. To overcome this difficulty we develop a multi-scale mathematical model which provides a clear framework to explore these connections across biological scales. Starting with an individual-based mechanical model of cell movement, we subsequently derive a novel coarse-grained system of partial differential equations governing the evolution of the cell density due to heterogeneous cellular properties. We demonstrate that solutions of the individual-based model converge to numerical solutions of the coarse-grained model, for both slowly-varying-in-space and rapidly-varying-in-space cellular properties. Applications of the model are discussed, including determining relative cellular-level properties and an interpretation of data from a breast cancer detection experiment.


2013 ◽  
Vol 46 (1) ◽  
pp. 417-430 ◽  
Author(s):  
Prakash Chandra Mohanty ◽  
Ranganalli Somashekharappa Mahendra ◽  
Hrusikesh Bisoyi ◽  
Srinivasa Kumar Tummula ◽  
George Grinson ◽  
...  

2001 ◽  
Vol 2001 (1) ◽  
Author(s):  
J. Maynard Smith

Aging processes are defined as those that increase the susceptibility of individuals as they grow older to the factors that may cause death. Various possible theories of aging are considered, and evidence that may help to decide between them is discussed. Changes in different organ systems may be merely symptoms of some single aging process, or they may be largely independent and synchronized by natural selection. Even if different organ systems age independently, they may do so as a result of similar changes at a cellular level. Cellular theories of aging may have to take into account the effects of selection between the cells in a tissue. The effects of radiation and somatic mutation theories of aging are discussed. It is suggested that radiation shortens life by inducing somatic mutations but that normal aging is not to any important extent caused by somatic mutations, although it may result from changes in cells that have effects on the physiology of the individual similar to those of somatic mutations. Evidence is presented that in Drosophila and in mice there are two phases in the life-span. In Drosophila , there is an initial “aging” phase, which is irreversible and occurs at a rate approximately independent of temperature, and a second “dying” phase, which is temperature-dependent in rate and reversible at lower temperatures. Reproduced by permission. J. Maynard Smith, Review Lectures on Senescence: I. The Causes of Aging. Proc. R. Soc. London Ser. B 157 , 115-127 (1962).


2020 ◽  
Vol 295 (10) ◽  
pp. 3064-3079 ◽  
Author(s):  
Manuel Iburg ◽  
Dmytro Puchkov ◽  
Irving U. Rosas-Brugada ◽  
Linda Bergemann ◽  
Ulrike Rieprecht ◽  
...  

Small heat shock proteins (sHsps) are conserved, ubiquitous members of the proteostasis network. Canonically, they act as “holdases” and buffer unfolded or misfolded proteins against aggregation in an ATP-independent manner. Whereas bacteria and yeast each have only two sHsps in their genomes, this number is higher in metazoan genomes, suggesting a spatiotemporal and functional specialization in higher eukaryotes. Here, using recombinantly expressed and purified proteins, static light-scattering analysis, and disaggregation assays, we report that the noncanonical sHsp HSP-17 of Caenorhabditis elegans facilitates aggregation of model substrates, such as malate dehydrogenase (MDH), and inhibits disaggregation of luciferase in vitro. Experiments with fluorescently tagged HSP-17 under the control of its endogenous promoter revealed that HSP-17 is expressed in the digestive and excretory organs, where its overexpression promotes the aggregation of polyQ proteins and of the endogenous kinase KIN-19. Systemic depletion of hsp-17 shortens C. elegans lifespan and severely reduces fecundity and survival upon prolonged heat stress. HSP-17 is an abundant protein exhibiting opposing chaperone activities on different substrates, indicating that it is a selective protein aggregase with physiological roles in development, digestion, and osmoregulation.


2004 ◽  
Vol 61 (5) ◽  
pp. 673-684 ◽  
Author(s):  
Rafel Simó

Major advances in dimethylated sulfur research are being made by approaching its dynamics at multiple scales. At the molecular to cellular level, single-cell techniques in molecular biology allow us to identify the microbes involved in cycling of dimethylated sulfur. Also, we find that dimethylsulfoxide (DMSO) is as ubiquitous as dimethyl sulfoniopropionate (DMSP) in marine plankton, which supports the recent suggestion that both compounds are involved in coping with oxidative stress. At the community level, there is recent evidence for the role of DMSP as a major carrier in organic sulfur transfer and cycling through trophic levels, from phytoplankton to bacteria and to zooplankton through herbivore protozoans. As a consequence, the food web dynamics drive the oceanic emission of atmospheric sulfur. At the ecosystem level, the diverse and intricate effects of the physicochemical setting (light, wind, nutrients) on the oceanic cycling of dimethylated sulfur are being uncovered. A proposed shortcut to detailed understanding of the individual processes presents the depth of the surface mixed layer as the variable that integrates most of the environmental effects and serves for predicting dimethylsulfide (DMS) concentrations, even at the global ocean level. This opens the door to assessing the strength of the DMS biogeophysical system as a climate regulator.


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