The cell physiology of coral bleaching

2006 ◽  
pp. 55-71 ◽  
Author(s):  
Sophie G. Dove ◽  
Ove Hoegh-Guldberg
Keyword(s):  
Coral Bleaching ◽  
Cell Physiology

Predicting cold-water bleaching in corals: role of temperature, and potential integration of light exposure

2020 ◽  
Vol 642 ◽  
pp. 133-146
Author(s):  
PC González-Espinosa ◽  
SD Donner
Keyword(s):  
Coral Bleaching ◽  
Cold Water ◽  
Light Exposure ◽  
Light Attenuation ◽  
Florida Keys ◽  
Cold Temperature ◽  
Warm Water ◽  
Coral Tissue ◽  
Effect Of Temperature ◽  
Type I

Warm-water growth and survival of corals are constrained by a set of environmental conditions such as temperature, light, nutrient levels and salinity. Water temperatures of 1 to 2°C above the usual summer maximum can trigger a phenomenon known as coral bleaching, whereby disruption of the symbiosis between coral and dinoflagellate micro-algae, living within the coral tissue, reveals the white skeleton of coral. Anomalously cold water can also lead to coral bleaching but has been the subject of limited research. Although cold-water bleaching events are less common, they can produce similar impacts on coral reefs as warm-water events. In this study, we explored the effect of temperature and light on the likelihood of cold-water coral bleaching from 1998-2017 using available bleaching observations from the Eastern Tropical Pacific and the Florida Keys. Using satellite-derived sea surface temperature, photosynthetically available radiation and light attenuation data, cold temperature and light exposure metrics were developed and then tested against the bleaching observations using logistic regression. The results show that cold-water bleaching can be best predicted with an accumulated cold-temperature metric, i.e. ‘degree cooling weeks’, analogous to the heat stress metric ‘degree heating weeks’, with high accuracy (90%) and fewer Type I and Type II errors in comparison with other models. Although light, when also considered, improved prediction accuracy, we found that the most reliable framework for cold-water bleaching prediction may be based solely on cold-temperature exposure.

Applications of multi-photon microscopy in cell physiology

10.2741/1353 ◽  
2004 ◽  
Vol 9 (1-3) ◽  
pp. 1598 ◽  
Author(s):  
Ernst Niggli
Keyword(s):  
Cell Physiology

MicroRNAs as Biomarker for Breast Cancer

2020 ◽  
Vol 20 (10) ◽  
pp. 1597-1610 ◽  
Author(s):  
Taru Aggarwal ◽  
Ridhima Wadhwa ◽  
Riya Gupta ◽  
Keshav Raj Paudel ◽  
Trudi Collet ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Association Studies ◽  
Large Family ◽  
Breast Cancer Diagnosis ◽  
Cell Multiplication ◽  
Cell Physiology ◽  
Gene Transcript ◽  
Genome Wide Association Studies ◽  
Non Coding Rnas

Regardless of advances in detection and treatment, breast cancer affects about 1.5 million women all over the world. Since the last decade, genome-wide association studies (GWAS) have been extensively conducted for breast cancer to define the role of miRNA as a tool for diagnosis, prognosis and therapeutics. MicroRNAs are small, non-coding RNAs that are associated with the regulation of key cellular processes such as cell multiplication, differentiation, and death. They cause a disturbance in the cell physiology by interfering directly with the translation and stability of a targeted gene transcript. MicroRNAs (miRNAs) constitute a large family of non-coding RNAs, which regulate target gene expression and protein levels that affect several human diseases and are suggested as the novel markers or therapeutic targets, including breast cancer. MicroRNA (miRNA) alterations are not only associated with metastasis, tumor genesis but also used as biomarkers for breast cancer diagnosis or prognosis. These are explained in detail in the following review. This review will also provide an impetus to study the role of microRNAs in breast cancer.

scholarly journals Lysosomes, Autophagy, and Hormesis in Cell Physiology, Pathology, and Age-Related Disease

Dose-Response ◽  
2020 ◽  
Vol 18 (3) ◽  
pp. 155932582093422 ◽  
Author(s):  
Michael N. Moore
Keyword(s):  
Intracellular Signaling ◽  
Adenosine Monophosphate ◽  
Target Of Rapamycin ◽  
Cell Physiology ◽  
Mechanistic Target Of Rapamycin ◽  
Age Related ◽  
Mechanistic Basis ◽  
The Many ◽  
Mtor Complex 1

Autophagy has been strongly linked with hormesis, however, it is only relatively recently that the mechanistic basis underlying this association has begun to emerge. Lysosomal autophagy is a group of processes that degrade proteins, protein aggregates, membranes, organelles, segregated regions of cytoplasm, and even parts of the nucleus in eukaryotic cells. These degradative processes are evolutionarily very ancient and provide a survival capability for cells that are stressed or injured. Autophagy and autophagic dysfunction have been linked with many aspects of cell physiology and pathology in disease processes; and there is now intense interest in identifying various therapeutic strategies involving its regulation. The main regulatory pathway for augmented autophagy is the mechanistic target of rapamycin (mTOR) cell signaling, although other pathways can be involved, such as 5′-adenosine monophosphate-activated protein kinase. Mechanistic target of rapamycin is a key player in the many highly interconnected intracellular signaling pathways and is responsible for the control of cell growth among other processes. Inhibition of mTOR (specifically dephosphorylation of mTOR complex 1) triggers augmented autophagy and the search is on the find inhibitors that can induce hormetic responses that may be suitable for treating many diseases, including many cancers, type 2 diabetes, and age-related neurodegenerative conditions.

scholarly journals Methionine Diet Evoked Hyperhomocysteinemia Causes Hippocampal Alterations, Metabolomics Plasma Changes and Behavioral Pattern in Wild Type Rats

2021 ◽  
Vol 22 (9) ◽  
pp. 4961
Author(s):  
Maria Kovalska ◽  
Eva Baranovicova ◽  
Dagmar Kalenska ◽  
Anna Tomascova ◽  
Marian Adamkov ◽  
...  
Keyword(s):  
Morphological Changes ◽  
Brain Area ◽  
Critical Role ◽  
Cerebrovascular Diseases ◽  
Behavioral Pattern ◽  
Cell Physiology ◽  
Male Wistar Rats ◽  
High Level ◽  
Hippocampal Alterations ◽  
The Impact

L-methionine, an essential amino acid, plays a critical role in cell physiology. High intake and/or dysregulation in methionine (Met) metabolism results in accumulation of its intermediate(s) or breakdown products in plasma, including homocysteine (Hcy). High level of Hcy in plasma, hyperhomocysteinemia (hHcy), is considered to be an independent risk factor for cerebrovascular diseases, stroke and dementias. To evoke a mild hHcy in adult male Wistar rats we used an enriched Met diet at a dose of 2 g/kg of animal weight/day in duration of 4 weeks. The study contributes to the exploration of the impact of Met enriched diet inducing mild hHcy on nervous tissue by detecting the histo-morphological, metabolomic and behavioural alterations. We found an altered plasma metabolomic profile, modified spatial and learning memory acquisition as well as remarkable histo-morphological changes such as a decrease in neurons’ vitality, alterations in the morphology of neurons in the selective vulnerable hippocampal CA 1 area of animals treated with Met enriched diet. Results of these approaches suggest that the mild hHcy alters plasma metabolome and behavioural and histo-morphological patterns in rats, likely due to the potential Met induced changes in “methylation index” of hippocampal brain area, which eventually aggravates the noxious effect of high methionine intake.

scholarly journals Inhibition of mitochondrial function by metformin increases glucose uptake, glycolysis and GDF-15 release from intestinal cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ming Yang ◽  
Tamana Darwish ◽  
Pierre Larraufie ◽  
Debra Rimmington ◽  
Irene Cimino ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Glucose Uptake ◽  
Intestinal Cell ◽  
Cell Physiology ◽  
Sequencing Analysis ◽  
Extracellular Acidification ◽  
Type2 Diabetes ◽  
Site Of Action ◽  
Glycolytic Rate ◽  
Hexose Metabolism

AbstractEven though metformin is widely used to treat type2 diabetes, reducing glycaemia and body weight, the mechanisms of action are still elusive. Recent studies have identified the gastrointestinal tract as an important site of action. Here we used intestinal organoids to explore the effects of metformin on intestinal cell physiology. Bulk RNA-sequencing analysis identified changes in hexose metabolism pathways, particularly glycolytic genes. Metformin increased expression of Slc2a1 (GLUT1), decreased expression of Slc2a2 (GLUT2) and Slc5a1 (SGLT1) whilst increasing GLUT-dependent glucose uptake and glycolytic rate as observed by live cell imaging of genetically encoded metabolite sensors and measurement of oxygen consumption and extracellular acidification rates. Metformin caused mitochondrial dysfunction and metformin’s effects on 2D-cultures were phenocopied by treatment with rotenone and antimycin-A, including upregulation of GDF15 expression, previously linked to metformin dependent weight loss. Gene expression changes elicited by metformin were replicated in 3D apical-out organoids and distal small intestines of metformin treated mice. We conclude that metformin affects glucose uptake, glycolysis and GDF-15 secretion, likely downstream of the observed mitochondrial dysfunction. This may explain the effects of metformin on intestinal glucose utilisation and food balance.

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