Faculty Opinions recommendation of Epigenetic control of rDNA loci in response to intracellular energy status.

2008 ◽  
Author(s):  
Lucio Comai
Keyword(s):  
Energy Status ◽  
Epigenetic Control ◽  
Rdna Loci ◽  
Intracellular Energy

scholarly journals Epigenetic Control of rDNA Loci in Response to Intracellular Energy Status

Cell ◽  
2008 ◽  
Vol 133 (4) ◽  
pp. 627-639 ◽  
Author(s):  
Akiko Murayama ◽  
Kazuji Ohmori ◽  
Akiko Fujimura ◽  
Hiroshi Minami ◽  
Kayoko Yasuzawa-Tanaka ◽  
...  
Keyword(s):  
Energy Status ◽  
Epigenetic Control ◽  
Rdna Loci ◽  
Intracellular Energy

scholarly journals Mitochondria surveillance systems trigger innate immune responses to bacterial pathogens via AMPK pathway in C. elegans

2020 ◽  
Author(s):  
Shouyong Ju ◽  
Hanqiao Chen ◽  
Shaoying Wang ◽  
Jian Lin ◽  
Raffi V Aroian ◽  
...  
Keyword(s):  
Immune System ◽  
Immune Responses ◽  
Innate Immune ◽  
Surveillance Systems ◽  
Innate Immune Responses ◽  
Energy Status ◽  
Microbial Infection ◽  
C Elegans ◽  
Host Interaction ◽  
Intracellular Energy

AbstractPathogen recognition and triggering pattern of host innate immune system is critical to understanding pathogen-host interaction. It is generally accepted that the microbial infection can be recognized by host via pattern-triggered immunity (PTI) or effector-triggered immunity (ETI) responses. Recently, non-PRR-mediated cellular surveillance systems have been reported as an important supplement strategy to PTI and ETI responses. However, the mechanism of how surveillance systems sense pathogens and trigger innate immune responses is largely unknown. In the present study, using Bacillus thuringiensis-Caenorhabditis elegans as a model, we found a new approach for surveillance systems to sense the pathogens through no-PPRs patterns. We reported C. elegans can monitor intracellular energy status through the mitochondrial surveillance system to triggered innate immune responses against pathogenic attack via AMP-activated protein kinase (AMPK). Consider that the mitochondria surveillance systems and AMPK are conserved components from worms to mammals, our study suggests that disrupting mitochondrial homeostasis to activate the immune system through AMPK-dependent pathways may widely existing in animals.

Enhancement of antitumor activity by epigenetic regulation of tumour-specific T cells

Impact ◽  
2021 ◽  
Vol 2021 (8) ◽  
pp. 6-8
Author(s):  
Takeshi Yamada ◽  
Yuya Arakawa
Keyword(s):  
T Cells ◽  
T Cell ◽  
Energy Metabolism ◽  
T Cell Differentiation ◽  
Glutamine Metabolism ◽  
T Cell Exhaustion ◽  
Epigenetic Changes ◽  
Cell Exhaustion ◽  
Epigenetic Control ◽  
Intracellular Energy

Adoptive immunotherapy can be used to treat intractable cancers but this involves taking T cells from a patient and growing them in a laboratory and, once outside the body, the T cells can fall into a state of exhaustion. This is a barrier that Professor Takeshi Yamada, Department of Medical Technology, Immunology, Ehime Prefectural University of Health Sciences, Japan, is seeking to overcome. His work involves establishing a better understanding of the mechanisms of T cell exhaustion, which are currently not well known. Yamada and his team are focusing on intracellular energy metabolism and epigenetic control in mouse models with a view to finding a way to inhibit T cell exhaustion. The researchers are developing protocols to improve T cell function for immunotherapy by controlling epigenetic changes involved in glutamine metabolism, which induces T cell exhaustion. As previous research has focused on activating and proliferating tumour-specific T cells, Yamada's approach, with a focus on epigenetic control, is novel. The team is interested in T cell differentiation and its links to T cell exhaustion and so they are exploring the mechanism of T cell differentiation via intracellular energy metabolism and epigenetic changes and how this can impact on exhaustion. The researchers previously clarified that the enhancement of glutamine metabolism that occurs during the activation of T cell cultures causes epigenetic changes that induce T cell exhaustion and are expanding on this finding in order to develop a method to suppress T cell exhaustion via epigenetic control.

scholarly journals Adenosine and ATP-sensitive potassium channels modulate dopamine release in the anoxic turtle (Trachemys scripta) striatum

2005 ◽  
Vol 289 (1) ◽  
pp. R77-R83 ◽  
Author(s):  
Sarah L. Milton ◽  
Peter L. Lutz
Keyword(s):  
Dopamine Release ◽  
Trachemys Scripta ◽  
Mammalian Brain ◽  
Freshwater Turtle ◽  
Energy Status ◽  
Gbr 12909 ◽  
Butanedione Monoxime ◽  
Intracellular Energy

Excessive dopamine (DA) is known to cause hypoxic/ischemic damage to mammalian brain. The freshwater turtle Trachemys scripta, however, maintains basal striatal DA levels in anoxia. We investigated DA balance during early anoxia when energy status in the turtle brain is compromised. The roles of ATP-sensitive potassium (KATP) channels and adenosine (AD) receptors were investigated as these factors affect DA balance in mammalian neurons. Striatal extracellular DA was determined by microdialysis with HPLC in the presence or absence of the specific DA transport blocker GBR-12909, the KATP blocker 2,3-butanedione monoxime, or the nonspecific AD receptor blocker theophylline. We found that in contrast to long-term anoxia, blocking DA reuptake did not significantly increase extracellular levels in 1-h anoxic turtles. Low DA levels in early anoxia were maintained instead by activation of KATP channels and AD receptors. Blocking KATP resulted in a 227% increase in extracellular DA in 1-h anoxic turtles but had no effect after 4 h of anoxia. Similarly, blocking AD receptors increased DA during the first hour of anoxia but did not change DA levels at 4-h anoxia. Support for the role of KATP channels in DA balance comes from normoxic animals treated with KATP opener; infusing diazoxide but not adenosine into the normoxic turtle striatum resulted in an immediate DA decrease to 14% of basal values within 1.5 h. Alternative strategies to maintain low extracellular levels may prevent catastrophic DA increases when intracellular energy is compromised while permitting the turtle to maintain a functional neuronal network during long-term anoxia.

scholarly journals Coupling metabolism and chemotaxis-dependent behaviours by energy taxis receptors

Microbiology ◽  
2010 ◽  
Vol 156 (8) ◽  
pp. 2283-2293 ◽  
Author(s):  
Gladys Alexandre
Keyword(s):  
Bacterial Species ◽  
Energy Status ◽  
Chemical Parameters ◽  
Directed Movement ◽  
Energy Taxis ◽  
Physico Chemical ◽  
Dependent Form ◽  
Energy Sensing ◽  
Metabolic Activities ◽  
Intracellular Energy

Bacteria have evolved the ability to monitor changes in various physico-chemical parameters and to adapt their physiology and metabolism by implementing appropriate cellular responses to these changes. Energy taxis is a metabolism-dependent form of taxis and is the directed movement of motile bacteria in gradients of physico-chemical parameters that affect metabolism. Energy taxis has been described in diverse bacterial species and several dedicated energy sensors have been identified. The molecular mechanism of energy taxis has not been studied in as much detail as chemotaxis, but experimental evidence indicates that this behaviour differs from metabolism-independent taxis only by the presence of dedicated energy taxis receptors. Energy taxis receptors perceive changes in energy-related parameters, including signals related to the redox and/or intracellular energy status of the cell. The best-characterized energy taxis receptors are those that sense the redox state of the electron transport chain via non-covalently bound FAD cofactors. Other receptors shown to mediate energy taxis lack any recognizable redox cofactor or conserved energy-sensing motif, and some have been suggested to monitor changes in the proton motive force. The exact energy-sensing mechanism(s) involved are yet to be elucidated for most of these energy sensors. By monitoring changes in energy-related parameters, energy taxis receptors allow cells to couple motility behaviour with metabolism under diverse environmental conditions. Energy taxis receptors thus provide fruitful models to decipher how cells integrate sensory behaviours with metabolic activities.

scholarly journals Novel Nucleolar Pathway Connecting Intracellular Energy Status with p53 Activation

2011 ◽  
Vol 286 (23) ◽  
pp. 20861-20869 ◽  
Author(s):  
Takuya Kumazawa ◽  
Kazuho Nishimura ◽  
Takao Kuroda ◽  
Wakana Ono ◽  
Chie Yamaguchi ◽  
...  
Keyword(s):  
Energy Status ◽  
P53 Activation ◽  
Intracellular Energy

scholarly journals Synphilin-1 Binds ATP and Regulates Intracellular Energy Status

PLoS ONE ◽  
2014 ◽  
Vol 9 (12) ◽  
pp. e115233 ◽  
Author(s):  
Tianxia Li ◽  
Jingnan Liu ◽  
Wanli W. Smith
Keyword(s):  
Energy Status ◽  
Intracellular Energy

scholarly journals Relieving Cellular Energy Stress in Aging, Neurodegenerative, and Metabolic Diseases, SIRT1 as a Therapeutic and Promising Node

2021 ◽  
Vol 13 ◽  
Author(s):  
Yang Fang ◽  
Xifeng Wang ◽  
Danying Yang ◽  
Yimei Lu ◽  
Gen Wei ◽  
...  
Keyword(s):  
Neurodegenerative Diseases ◽  
Metabolic Diseases ◽  
Energy State ◽  
Energy Status ◽  
Atp Production ◽  
Energy Stress ◽  
Silent Information Regulator 1 ◽  
The Stability ◽  
Intracellular Energy ◽  
Expression And Activity

The intracellular energy state will alter under the influence of physiological or pathological stimuli. In response to this change, cells usually mobilize various molecules and their mechanisms to promote the stability of the intracellular energy status. Mitochondria are the main source of ATP. Previous studies have found that the function of mitochondria is impaired in aging, neurodegenerative diseases, and metabolic diseases, and the damaged mitochondria bring lower ATP production, which further worsens the progression of the disease. Silent information regulator-1 (SIRT1) is a multipotent molecule that participates in the regulation of important biological processes in cells, including cellular metabolism, cell senescence, and inflammation. In this review, we mainly discuss that promoting the expression and activity of SIRT1 contributes to alleviating the energy stress produced by physiological and pathological conditions. The review also discusses the mechanism of precise regulation of SIRT1 expression and activity in various dimensions. Finally, according to the characteristics of this mechanism in promoting the recovery of mitochondrial function, the relationship between current pharmacological preparations and aging, neurodegenerative diseases, metabolic diseases, and other diseases was analyzed.

scholarly journals Energetic limits to metabolic flexibility: responses of Saccharomyces cerevisiae to glucose–galactose transitions

Microbiology ◽  
2009 ◽  
Vol 155 (4) ◽  
pp. 1340-1350 ◽  
Author(s):  
J. van den Brink ◽  
M. Akeroyd ◽  
R. van der Hoeven ◽  
J. T. Pronk ◽  
J. H. de Winde ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Energy Charge ◽  
Metabolic Flexibility ◽  
Energy Status ◽  
Anaerobic Conditions ◽  
Leloir Pathway ◽  
Chemostat Cultures ◽  
Galactose Utilization ◽  
Intracellular Energy ◽  
Adenosine Nucleotide

Glucose is the favoured carbon source for Saccharomyces cerevisiae, and the Leloir pathway for galactose utilization is only induced in the presence of galactose during glucose-derepressed conditions. The goal of this study was to investigate the dynamics of glucose–galactose transitions. To this end, well-controlled, glucose-limited chemostat cultures were switched to galactose-excess conditions. Surprisingly, galactose was not consumed upon a switch to galactose excess under anaerobic conditions. However, the transcripts of the Leloir pathway were highly increased upon galactose excess under both aerobic and anaerobic conditions. Protein and enzyme-activity assays showed that impaired galactose consumption under anaerobiosis coincided with the absence of the Leloir-pathway proteins. Further results showed that absence of protein synthesis was not caused by glucose-mediated translation inhibition. Analysis of adenosine nucleotide pools revealed a fast decrease of the energy charge after the switch from glucose to galactose under anaerobic conditions. Similar results were obtained when glucose–galactose transitions were analysed under aerobic conditions with a respiratory-deficient strain. It is concluded that under fermentative conditions, the energy charge was too low to allow synthesis of the Leloir proteins. Hence, this study conclusively shows that the intracellular energy status is an important factor in the metabolic flexibility of S. cerevisiae upon changes in its environment.

scholarly journals Intracellular energy status regulates activity in hypocretin/orexin neurones: a link between energy and behavioural states

2011 ◽  
Vol 589 (17) ◽  
pp. 4157-4166 ◽  
Author(s):  
Zhong-Wu Liu ◽  
Geliang Gan ◽  
Shigetomo Suyama ◽  
Xiao-Bing Gao
Keyword(s):  
Energy Status ◽  
Intracellular Energy
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