scholarly journals Mitochondrial redox systems as central hubs in plant metabolism and signalling

2021 ◽  
Author(s):  
Olivier Van Aken
Keyword(s):  
Stress Responses ◽  
Plant Mitochondria ◽  
Nuclear Gene ◽  
Tca Cycle ◽  
Cellular Damage ◽  
Future Research ◽  
Antioxidant Systems ◽  
Plant Metabolism ◽  
Redox Systems ◽  
Glutathione Cycle

Abstract Plant mitochondria are indispensable for plant metabolism and are tightly integrated into cellular homeostasis. This review provides an update on the latest research concerning the organisation and operation of plant mitochondrial redox systems, and how they affect cellular metabolism and signalling, plant development and stress responses. New insights into the organisation and operation of mitochondrial energy systems such as the tricarboxylic acid (TCA) cycle and mitochondrial electron chain (mtETC) are discussed. The mtETC produces reactive oxygen and nitrogen species, which can act as signals or lead to cellular damage, and are thus efficiently removed by mitochondrial antioxidant systems, including Mn-superoxide dismutase, ascorbate-glutathione cycle and thioredoxin-dependent peroxidases. Plant mitochondria are tightly connected with photosynthesis, photorespiration and cytosolic metabolism, thereby providing redox-balancing. Mitochondrial proteins are targets of extensive post-translational modifications, but their functional significance and how they are added or removed remains unclear. To operate in sync with the whole cell, mitochondria can communicate their functional status via mitochondrial retrograde signalling to change nuclear gene expression, and several recent breakthroughs here are discussed. At a whole organism level, plant mitochondria thus play crucial roles from the first minutes after seed imbibition, supporting meristem activity, growth and fertility, until senescence of darkened and aged tissue. Finally, plant mitochondria are tightly integrated with cellular and organismal responses to environmental challenges such as drought, salinity, heat and submergence, but also threats posed by pathogens. Both the major recent advances and outstanding questions are reviewed, which may help future research efforts on plant mitochondria.

scholarly journals Nucleoredoxin guards against oxidative stress by protecting antioxidant enzymes

2017 ◽  
Vol 114 (31) ◽  
pp. 8414-8419 ◽  
Author(s):  
Sophie Kneeshaw ◽  
Rumana Keyani ◽  
Valérie Delorme-Hinoux ◽  
Lisa Imrie ◽  
Gary J. Loake ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stress Responses ◽  
Cellular Damage ◽  
Antioxidant Systems ◽  
Oxygen Species ◽  
Optimal Activity ◽  
Substrate Interaction ◽  
Wide Range ◽  
Scavenging Enzymes ◽  
Reduced State

Cellular accumulation of reactive oxygen species (ROS) is associated with a wide range of developmental and stress responses. Although cells have evolved to use ROS as signaling molecules, their chemically reactive nature also poses a threat. Antioxidant systems are required to detoxify ROS and prevent cellular damage, but little is known about how these systems manage to function in hostile, ROS-rich environments. Here we show that during oxidative stress in plant cells, the pathogen-inducible oxidoreductase Nucleoredoxin 1 (NRX1) targets enzymes of major hydrogen peroxide (H2O2)-scavenging pathways, including catalases. Mutant nrx1 plants displayed reduced catalase activity and were hypersensitive to oxidative stress. Remarkably, catalase was maintained in a reduced state by substrate-interaction with NRX1, a process necessary for its H2O2-scavenging activity. These data suggest that unexpectedly H2O2-scavenging enzymes experience oxidative distress in ROS-rich environments and require reductive protection from NRX1 for optimal activity.

scholarly journals Can neuroscience help to understand narcissism? A systematic review of an emerging field

2021 ◽  
Vol 4 ◽  
Author(s):  
Emanuel Jauk ◽  
Philipp Kanske
Keyword(s):  
Systematic Review ◽  
Stress Responses ◽  
Interpersonal Functioning ◽  
Integrative Model ◽  
Experimental Investigations ◽  
Future Research ◽  
Pathological Narcissism ◽  
Ego Threat ◽  
Self Reports ◽  
And Behavior

Abstract Narcissism is a Janusian personality construct, associated with both grandiose self-assuredness and dominance, as well as vulnerable insecurity and reactivity. Central questions of intra- and interpersonal functioning in narcissism are still a matter of debate. Neuroscience could help to understand the paradoxical patterns of experience and behavior beyond the limitations of self-reports. We provide a systematic review of 34 neuroscience studies on grandiose, vulnerable, pathological narcissism, and Narcissistic Personality Disorder (NPD), spanning experimental investigations of intra- and interpersonal mechanisms, research on neurophysiological and neuroendocrine aspects of baseline function, and brain structural correlates. While neuroscience has scarcely directly studied vulnerable narcissism, grandiose narcissism is associated with heightened vigilance to ego threat and stress responses following ego threat, as well as heightened stress indicators in baseline measures. Such responses are not commonly observed in self-reports, highlighting the potential of neuroscience to augment our understanding of self-regulatory dynamics in narcissism. Interpersonal functioning is characterized by deficits in social–affective processes. Both involve altered activity within the salience network, pointing to a double dissociation regarding the expression of narcissism and self/other oriented situational focus. Findings are summarized in an integrative model providing testable hypotheses for future research along with methodological recommendations.

scholarly journals Crosstalk between endoplasmic reticulum stress and oxidative stress: a dynamic duo in multiple myeloma

2021 ◽  
Author(s):  
Sinan Xiong ◽  
Wee-Joo Chng ◽  
Jianbiao Zhou
Keyword(s):  
Oxidative Stress ◽  
Multiple Myeloma ◽  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Cell Fate ◽  
Stress Responses ◽  
Plasma Cells ◽  
Reactive Oxygen Species Generation ◽  
Future Research ◽  
And Oxidative Stress

AbstractUnder physiological and pathological conditions, cells activate the unfolded protein response (UPR) to deal with the accumulation of unfolded or misfolded proteins in the endoplasmic reticulum. Multiple myeloma (MM) is a hematological malignancy arising from immunoglobulin-secreting plasma cells. MM cells are subject to continual ER stress and highly dependent on the UPR signaling activation due to overproduction of paraproteins. Mounting evidence suggests the close linkage between ER stress and oxidative stress, demonstrated by overlapping signaling pathways and inter-organelle communication pivotal to cell fate decision. Imbalance of intracellular homeostasis can lead to deranged control of cellular functions and engage apoptosis due to mutual activation between ER stress and reactive oxygen species generation through a self-perpetuating cycle. Here, we present accumulating evidence showing the interactive roles of redox homeostasis and proteostasis in MM pathogenesis and drug resistance, which would be helpful in elucidating the still underdefined molecular pathways linking ER stress and oxidative stress in MM. Lastly, we highlight future research directions in the development of anti-myeloma therapy, focusing particularly on targeting redox signaling and ER stress responses.

scholarly journals LONP1 and ClpP cooperatively regulate mitochondrial proteostasis for cancer cell survival

Oncogenesis ◽  
2021 ◽  
Vol 10 (2) ◽  
Author(s):  
Yu Geon Lee ◽  
Hui Won Kim ◽  
Yeji Nam ◽  
Kyeong Jin Shin ◽  
Yu Jin Lee ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Growth ◽  
Cell Survival ◽  
Cancer Cell ◽  
Stress Responses ◽  
Molecular Mechanisms ◽  
Tca Cycle ◽  
Mitochondrial Matrix ◽  
Mitochondrial Functions ◽  
Cancer Cell Survival

AbstractMitochondrial proteases are key components in mitochondrial stress responses that maintain proteostasis and mitochondrial integrity in harsh environmental conditions, which leads to the acquisition of aggressive phenotypes, including chemoresistance and metastasis. However, the molecular mechanisms and exact role of mitochondrial proteases in cancer remain largely unexplored. Here, we identified functional crosstalk between LONP1 and ClpP, which are two mitochondrial matrix proteases that cooperate to attenuate proteotoxic stress and protect mitochondrial functions for cancer cell survival. LONP1 and ClpP genes closely localized on chromosome 19 and were co-expressed at high levels in most human cancers. Depletion of both genes synergistically attenuated cancer cell growth and induced cell death due to impaired mitochondrial functions and increased oxidative stress. Using mitochondrial matrix proteomic analysis with an engineered peroxidase (APEX)-mediated proximity biotinylation method, we identified the specific target substrates of these proteases, which were crucial components of mitochondrial functions, including oxidative phosphorylation, the TCA cycle, and amino acid and lipid metabolism. Furthermore, we found that LONP1 and ClpP shared many substrates, including serine hydroxymethyltransferase 2 (SHMT2). Inhibition of both LONP1 and ClpP additively increased the amount of unfolded SHMT2 protein and enhanced sensitivity to SHMT2 inhibitor, resulting in significantly reduced cell growth and increased cell death under metabolic stress. Additionally, prostate cancer patients with higher LONP1 and ClpP expression exhibited poorer survival. These results suggest that interventions targeting the mitochondrial proteostasis network via LONP1 and ClpP could be potential therapeutic strategies for cancer.

scholarly journals Developmental Origins of Kidney Disease: Why Oxidative Stress Matters?

Antioxidants ◽  
2020 ◽  
Vol 10 (1) ◽  
pp. 33
Author(s):  
Chien-Ning Hsu ◽  
You-Lin Tain
Keyword(s):  
Oxidative Stress ◽  
Kidney Disease ◽  
Current Knowledge ◽  
Future Research ◽  
Antioxidant Systems ◽  
Developmental Origins ◽  
Adult Onset ◽  
Functional Changes ◽  
Health And Disease ◽  
Developing Kidney

The “developmental origins of health and disease” theory indicates that many adult-onset diseases can originate in the earliest stages of life. The developing kidney has emerged as being particularly vulnerable to adverse in utero conditions leading to morphological and functional changes, namely renal programming. Emerging evidence indicates oxidative stress, an imbalance between reactive oxygen/nitrogen species (ROS/RNS) and antioxidant systems, plays a pathogenetic role in the developmental programming of kidney disease. Conversely, perinatal use of antioxidants has been implemented to reverse programming processes and prevent adult-onset diseases. We have termed this reprogramming. The focus of this review is twofold: (1) To summarize the current knowledge on oxidative stress implicated in renal programming and kidney disease of developmental origins; and (2) to provide an overview of reprogramming effects of perinatal antioxidant therapy on renal programming and how this may prevent adult-onset kidney disease. Although early-life oxidative stress is implicated in mediating renal programming and adverse offspring renal outcomes, and animal models provide promising results to allow perinatal antioxidants applied as potential reprogramming interventions, it is still awaiting clinical translation. This presents exciting new challenges and areas for future research.

MondoA Drives B-ALL Malignancy through Enhanced Adaptation to Metabolic Stress

Blood ◽  
2021 ◽  
Author(s):  
Alexandra Sipol ◽  
Erik Hameister ◽  
Busheng Xue ◽  
Julia Hofstetter ◽  
Maxim Barenboim ◽  
...  
Keyword(s):  
Stress Responses ◽  
Lymphoblastic Leukemia ◽  
Metabolic Stress ◽  
Tca Cycle ◽  
Underlying Mechanism ◽  
Patient Data ◽  
Data Sets ◽  
Dependent Manner

Cancer cells are in most instances characterized by rapid proliferation and uncontrolled cell division. Hence, they must adapt to proliferation-induced metabolic stress through intrinsic or acquired anti-metabolic stress responses to maintain homeostasis and survival. One mechanism to achieve this is to reprogram gene expression in a metabolism-dependent manner. MondoA (also known as MLXIP), a member of the MYC interactome, has been described as an example of such a metabolic sensor. However, the role of MondoA in malignancy is not fully understood and the underlying mechanism in metabolic responses remains elusive. By assessing patient data sets we found that MondoA overexpression is associated with a worse survival in pediatric common acute lymphoblastic leukemia (B-ALL). Using CRISPR/Cas9 and RNA interference approaches, we observed that MondoA depletion reduces transformational capacity of B-ALL cells in vitro and dramatically inhibits malignant potential in an in vivo mouse model. Interestingly, reduced expression of MondoA in patient data sets correlated with enrichment in metabolic pathways. The loss of MondoA correlated with increased tricarboxylic acid (TCA) cycle activity. Mechanistically, MondoA senses metabolic stress in B-ALL cells by restricting oxidative phosphorylation through reduced PDH activity. Glutamine starvation conditions greatly enhance this effect and highlight the inability to mitigate metabolic stress upon loss of MondoA in B-ALL. Our findings give a novel insight into the function of MondoA in pediatric B-ALL and support the notion that MondoA inhibition in this entity offers a therapeutic opportunity and should be further explored.

scholarly journals Epigenetic Responses to Temperature and Climate

2020 ◽  
Vol 60 (6) ◽  
pp. 1469-1480 ◽  
Author(s):  
Beth A McCaw ◽  
Tyler J Stevenson ◽  
Lesley T Lancaster
Keyword(s):  
Temperature Change ◽  
Stress Responses ◽  
Environmental Temperature ◽  
Environmental Control ◽  
Global Climate ◽  
Thermal Adaptation ◽  
Epigenetic Inheritance ◽  
Epigenetic Modifications ◽  
Future Research ◽  
Adaptation To Climate Change

Synopsis Epigenetics represents a widely accepted set of mechanisms by which organisms respond to the environment by regulating phenotypic plasticity and life history transitions. Understanding the effects of environmental control on phenotypes and fitness, via epigenetic mechanisms, is essential for understanding the ability of organisms to rapidly adapt to environmental change. This review highlights the significance of environmental temperature on epigenetic control of phenotypic variation, with the aim of furthering our understanding of how epigenetics might help or hinder species’ adaptation to climate change. It outlines how epigenetic modifications, including DNA methylation and histone/chromatin modification, (1) respond to temperature and regulate thermal stress responses in different kingdoms of life, (2) regulate temperature-dependent expression of key developmental processes, sex determination, and seasonal phenotypes, (3) facilitate transgenerational epigenetic inheritance of thermal adaptation, (4) adapt populations to local and global climate gradients, and finally (5) facilitate in biological invasions across climate regions. Although the evidence points towards a conserved role of epigenetics in responding to temperature change, there appears to be an element of temperature- and species-specificity in the specific effects of temperature change on epigenetic modifications and resulting phenotypic responses. The review identifies areas of future research in epigenetic responses to environmental temperature change.

scholarly journals Functions of PPR Proteins in Plant Growth and Development

2021 ◽  
Vol 22 (20) ◽  
pp. 11274
Author(s):  
Xiulan Li ◽  
Mengdi Sun ◽  
Shijuan Liu ◽  
Qian Teng ◽  
Shihui Li ◽  
...  
Keyword(s):  
Plant Growth ◽  
Stress Responses ◽  
Rna Processing ◽  
Growth And Development ◽  
Molecular Mechanisms ◽  
Rna Binding ◽  
Plant Mitochondria ◽  
Research Progress ◽  
Plant Growth And Development ◽  
Ppr Proteins

Pentatricopeptide repeat (PPR) proteins form a large protein family in land plants, with hundreds of different members in angiosperms. In the last decade, a number of studies have shown that PPR proteins are sequence-specific RNA-binding proteins involved in multiple aspects of plant organellar RNA processing, and perform numerous functions in plants throughout their life cycle. Recently, computational and structural studies have provided new insights into the working mechanisms of PPR proteins in RNA recognition and cytidine deamination. In this review, we summarized the research progress on the functions of PPR proteins in plant growth and development, with a particular focus on their effects on cytoplasmic male sterility, stress responses, and seed development. We also documented the molecular mechanisms of PPR proteins in mediating RNA processing in plant mitochondria and chloroplasts.

scholarly journals Molecular Evolution of Calcium Signaling and Transport in Plant Adaptation to Abiotic Stress

2021 ◽  
Vol 22 (22) ◽  
pp. 12308
Author(s):  
Tao Tong ◽  
Qi Li ◽  
Wei Jiang ◽  
Guang Chen ◽  
Dawei Xue ◽  
...  
Keyword(s):  
Abiotic Stress ◽  
Calcium Signaling ◽  
Stress Responses ◽  
Evolutionary Biology ◽  
Regulatory Networks ◽  
Cascade Reactions ◽  
Future Research ◽  
Spatiotemporal Pattern ◽  
Green Plants ◽  
Signaling Components

Adaptation to unfavorable abiotic stresses is one of the key processes in the evolution of plants. Calcium (Ca2+) signaling is characterized by the spatiotemporal pattern of Ca2+ distribution and the activities of multi-domain proteins in integrating environmental stimuli and cellular responses, which are crucial early events in abiotic stress responses in plants. However, a comprehensive summary and explanation for evolutionary and functional synergies in Ca2+ signaling remains elusive in green plants. We review mechanisms of Ca2+ membrane transporters and intracellular Ca2+ sensors with evolutionary imprinting and structural clues. These may provide molecular and bioinformatics insights for the functional analysis of some non-model species in the evolutionarily important green plant lineages. We summarize the chronological order, spatial location, and characteristics of Ca2+ functional proteins. Furthermore, we highlight the integral functions of calcium-signaling components in various nodes of the Ca2+ signaling pathway through conserved or variant evolutionary processes. These ultimately bridge the Ca2+ cascade reactions into regulatory networks, particularly in the hormonal signaling pathways. In summary, this review provides new perspectives towards a better understanding of the evolution, interaction and integration of Ca2+ signaling components in green plants, which is likely to benefit future research in agriculture, evolutionary biology, ecology and the environment.

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