scholarly journals A Metabolic Choreography of Maize Plants Treated with a Humic Substance-Based Biostimulant under Normal and Starved Conditions

Metabolites ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 403
Author(s):  
Kgalaletso Othibeng ◽  
Lerato Nephali ◽  
Anza-Tshilidzi Ramabulana ◽  
Paul Steenkamp ◽  
Daniel Petras ◽  
...  
Keyword(s):  
Humic Substance ◽  
Metabolic Networks ◽  
Molecular Mechanisms ◽  
Plant Cell Wall ◽  
Growth Promotion ◽  
Redox Homeostasis ◽  
Metabolic Reprogramming ◽  
Sustainable Food ◽  
Crop Development ◽  
Maize Plants

Humic substance (HS)-based biostimulants show potentials as sustainable strategies for improved crop development and stress resilience. However, cellular and molecular mechanisms governing the agronomically observed effects of HS on plants remain enigmatic. Here, we report a global metabolic reprogramming of maize leaves induced by a humic biostimulant under normal and nutrient starvation conditions. This reconfiguration of the maize metabolism spanned chemical constellations, as revealed by molecular networking approaches. Plant growth and development under normal conditions were characterized by key differential metabolic changes such as increased levels of amino acids, oxylipins and the tricarboxylic acid (TCA) intermediate, isocitric acid. Furthermore, under starvation, the humic biostimulant significantly impacted pathways that are involved in stress-alleviating mechanisms such as redox homeostasis, strengthening of the plant cell wall, osmoregulation, energy production and membrane remodelling. Thus, this study reveals that the humic biostimulant induces a remodelling of inter-compartmental metabolic networks in maize, subsequently readjusting the plant physiology towards growth promotion and stress alleviation. Such insights contribute to ongoing efforts in elucidating modes of action of biostimulants, generating fundamental scientific knowledge that is necessary for development of the biostimulant industry, for sustainable food security.

scholarly journals A Metabolomic Landscape of Maize Plants Treated With a Microbial Biostimulant Under Well-Watered and Drought Conditions

2021 ◽  
Vol 12 ◽  
Author(s):  
Lerato Nephali ◽  
Venessa Moodley ◽  
Lizelle Piater ◽  
Paul Steenkamp ◽  
Nombuso Buthelezi ◽  
...  
Keyword(s):  
Plant Growth ◽  
Plant Cell Wall ◽  
Growth Promotion ◽  
Redox Homeostasis ◽  
Resistance Mechanisms ◽  
Growth Stress ◽  
Metabolic Reprogramming ◽  
Sustainable Food ◽  
Drought Conditions ◽  
Maize Plants

Microbial plant biostimulants have been successfully applied to improve plant growth, stress resilience and productivity. However, the mechanisms of action of biostimulants are still enigmatic, which is the main bottleneck for the fully realization and implementation of biostimulants into the agricultural industry. Here, we report the elucidation of a global metabolic landscape of maize (Zea mays L) leaves in response to a microbial biostimulant, under well-watered and drought conditions. The study reveals that the increased pool of tricarboxylic acid (TCA) intermediates, alterations in amino acid levels and differential changes in phenolics and lipids are key metabolic signatures induced by the application of the microbial-based biostimulant. These reconfigurations of metabolism gravitate toward growth-promotion and defense preconditioning of the plant. Furthermore, the application of microbial biostimulant conferred enhanced drought resilience to maize plants via altering key metabolic pathways involved in drought resistance mechanisms such as the redox homeostasis, strengthening of the plant cell wall, osmoregulation, energy production and membrane remodeling. For the first time, we show key molecular events, metabolic reprogramming, activated by a microbial biostimulant for plant growth promotion and defense priming. Thus, these elucidated metabolomic insights contribute to ongoing efforts in decoding modes of action of biostimulants and generating fundamental scientific knowledgebase that is necessary for the development of the plant biostimulants industry, for sustainable food security.

scholarly journals Long-Lasting Primed State in Maize Plants: Salicylic Acid and Steroid Signaling Pathways as Key Players in the Early Activation of Immune Responses in Silks

2019 ◽  
Vol 32 (1) ◽  
pp. 95-106 ◽  
Author(s):  
Romina B Agostini ◽  
Agustina Postigo ◽  
Sebastian P. Rius ◽  
Gabriel E. Rech ◽  
Valeria A. Campos-Bermudez ◽  
...  
Keyword(s):  
Cell Wall ◽  
Salicylic Acid ◽  
Stress Responses ◽  
Molecular Mechanisms ◽  
Plant Cell Wall ◽  
Cell Structure ◽  
Regulatory Elements ◽  
Transcriptional Analysis ◽  
Systemic Resistance ◽  
Maize Plants

In the present study, we investigated the induced systemic resistance (ISR) activated by the beneficial fungus Trichoderma atroviride in maize plants, and the early immunological responses triggered after challenge with the ear rot pathogen Fusarium verticillioides. By transcriptional analysis, we were able to identify the gene core set specifically modulated in silks of maize plants expressing ISR. Our results showed that the main transcriptional reprogramming falls into genes involved in five main functional categories: cell structure or cell wall, amino acid and protein metabolism, stress responses, signaling, and transport. Among these ISR-related genes, it is important to highlight novel findings regarding hormone metabolism and signaling. The expression of hormone-dependent genes was in good agreement with the abscisic acid, jasmonic acid, and salicylic acid (SA) levels detected in the plants under study. The experimental design allowed the identification of novel regulatory elements related to a heightened state of defense in silks and suggests that steroids and SA are central components of a master regulatory network controlling the immunity of silks during ISR. The results presented also provide evidence about the molecular mechanisms used by maize silks against F. verticillioides to counteract pathogenic development and host invasion, including pathogenesis-related genes, plant cell-wall reinforcement, fungal cell-wall-degrading enzymes and secondary metabolism.

scholarly journals Metabolic Reprogramming in Gastric Cancer: Trojan Horse Effect

2022 ◽  
Vol 11 ◽  
Author(s):  
Yu-Ling Bin ◽  
Hong-Sai Hu ◽  
Feng Tian ◽  
Zhen-Hua Wen ◽  
Mei-Feng Yang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Metabolic Networks ◽  
Molecular Mechanisms ◽  
Aerobic Glycolysis ◽  
Survival Rates ◽  
Growth Factor Receptor ◽  
Developed Countries ◽  
Metabolic Reprogramming ◽  
Current Evidence ◽  
Treatment Regimens

Worldwide, gastric cancer (GC) represents the fifth most common cancer for incidence and the third leading cause of death in developed countries. Despite the development of combination chemotherapies, the survival rates of GC patients remain unsatisfactory. The reprogramming of energy metabolism is a hallmark of cancer, especially increased dependence on aerobic glycolysis. In the present review, we summarized current evidence on how metabolic reprogramming in GC targets the tumor microenvironment, modulates metabolic networks and overcomes drug resistance. Preclinical and clinical studies on the combination of metabolic reprogramming targeted agents and conventional chemotherapeutics or molecularly targeted treatments [including vascular endothelial growth factor receptor (VEGFR) and HER2] and the value of biomarkers are examined. This deeper understanding of the molecular mechanisms underlying successful pharmacological combinations is crucial in finding the best-personalized treatment regimens for cancer patients.

scholarly journals Targeting hypoxic tumor microenvironment in pancreatic cancer

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Jinxin Tao ◽  
Gang Yang ◽  
Wenchuan Zhou ◽  
Jiangdong Qiu ◽  
Guangyu Chen ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Progression ◽  
Stromal Cells ◽  
Molecular Mechanisms ◽  
Redox Homeostasis ◽  
Metabolic Reprogramming ◽  
Normal Tissues ◽  
Innovative Therapies ◽  
Hypoxic Tumor ◽  
Resistance To Chemotherapy

AbstractAttributable to its late diagnosis, early metastasis, and poor prognosis, pancreatic cancer remains one of the most lethal diseases worldwide. Unlike other solid tumors, pancreatic cancer harbors ample stromal cells and abundant extracellular matrix but lacks vascularization, resulting in persistent and severe hypoxia within the tumor. Hypoxic microenvironment has extensive effects on biological behaviors or malignant phenotypes of pancreatic cancer, including metabolic reprogramming, cancer stemness, invasion and metastasis, and pathological angiogenesis, which synergistically contribute to development and therapeutic resistance of pancreatic cancer. Through various mechanisms including but not confined to maintenance of redox homeostasis, activation of autophagy, epigenetic regulation, and those induced by hypoxia-inducible factors, intratumoral hypoxia drives the above biological processes in pancreatic cancer. Recognizing the pivotal roles of hypoxia in pancreatic cancer progression and therapies, hypoxia-based antitumoral strategies have been continuously developed over the recent years, some of which have been applied in clinical trials to evaluate their efficacy and safety in combinatory therapies for patients with pancreatic cancer. In this review, we discuss the molecular mechanisms underlying hypoxia-induced aggressive and therapeutically resistant phenotypes in both pancreatic cancerous and stromal cells. Additionally, we focus more on innovative therapies targeting the tumor hypoxic microenvironment itself, which hold great potential to overcome the resistance to chemotherapy and radiotherapy and to enhance antitumor efficacy and reduce toxicity to normal tissues.

Targeting PPARalpha in Alzheimer's Disease

2018 ◽  
Vol 15 (4) ◽  
pp. 345-354 ◽  
Author(s):  
Barbara D'Orio ◽  
Anna Fracassi ◽  
Maria Paola Cerù ◽  
Sandra Moreno
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Molecular Mechanisms ◽  
Redox Homeostasis ◽  
Antioxidant Response ◽  
Peroxisome Proliferator ◽  
Prevailing Paradigm

Background: The molecular mechanisms underlying Alzheimer's disease (AD) are yet to be fully elucidated. The so-called “amyloid cascade hypothesis” has long been the prevailing paradigm for causation of disease, and is today being revisited in relation to other pathogenic pathways, such as oxidative stress, neuroinflammation and energy dysmetabolism. The peroxisome proliferator-activated receptors (PPARs) are expressed in the central nervous system (CNS) and regulate many physiological processes, such as energy metabolism, neurotransmission, redox homeostasis, autophagy and cell cycle. Among the three isotypes (α, β/δ, γ), PPARγ role is the most extensively studied, while information on α and β/δ are still scanty. However, recent in vitro and in vivo evidence point to PPARα as a promising therapeutic target in AD. Conclusion: This review provides an update on this topic, focussing on the effects of natural or synthetic agonists in modulating pathogenetic mechanisms at AD onset and during its progression. Ligandactivated PPARα inihibits amyloidogenic pathway, Tau hyperphosphorylation and neuroinflammation. Concomitantly, the receptor elicits an enzymatic antioxidant response to oxidative stress, ameliorates glucose and lipid dysmetabolism, and stimulates autophagy.

High Altitude hypoxia

2020 ◽  
Vol 17 ◽  
Author(s):  
Asma Babar ◽  
Kifayatullah Mengal ◽  
Abdul Hanan Babar ◽  
Shixin Wu ◽  
Mujahid Ali Shah ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
High Altitude ◽  
Molecular Mechanisms ◽  
Strong Association ◽  
Haemoglobin Concentration ◽  
Metabolic Reprogramming ◽  
Molecular Networks ◽  
Whole Genome ◽  
Gene Expressions ◽  
Transcriptional Responses

: The world highest and largest altitude area is called the Qinghai-Tibetan plateau (QTB), which harbors unique animal and plant species. Mammals that inhabit the higher altitude regions have adapted well to the hypoxic conditions. One of the main stressors at high altitude is hypoxia. Metabolic responses to hypoxia play important roles in cell survival strategies and some diseases. However, the homeostatic alterations that equilibrate variations in the demand and supply of energy to maintain organismal function in a prolonged low O2 environment persist partly understood, making it problematic to differentiate adaptive from maladaptive responses in hypoxia. Tibetans and yaks are two perfect examples innate to the plateau for high altitude adaptation. By the scan of the whole-genome, EPAS1 and EGLN1 were identified as key genes associated with sustained haemoglobin concentration in high altitude mammals for adaptation. The yak is a much more ancient mammal which has existed on QTB longer than humans, it is, therefore, possible that natural selection represented a diverse group of genes/pathways in yaks. Physiological characteristics are extremely informative in revealing molecular networks associated with inherited adaptation, in addition to the whole-genome adaptive changes at the DNA sequence level. Gene-expression can be changed by a variety of signals originating from the environment, and hypoxia is the main factor amongst them. The hypoxia-inducible factors (HIF-1α and EPAS1/HIF-2α) are the main regulators of oxygen in homeostasis which play a role as maestro regulators of adaptation in hypoxic reaction of molecular mechanisms. (Vague) The basis of this review is to present recent information regarding the molecular mechanism involved in hypoxia that regulates candidate genes and proteins. Many transcriptional responses toward hypoxia are facilitated by HIFs that change the number of gene expressions and help in angiogenesis, erythropoiesis, metabolic reprogramming and metastasis. HIFs also activate several signals highlighting a strong association between hypoxia, the misfolded proteins’ accumulation in the endoplasmic reticulum in stress and activation of unfolded protein response (UPR). It was observed that at high-altitude, pregnancies yield a low birth weight ∼100 g per1000 m of the climb. (Vague) It may involve variation in the events of energy-demanding, like protein synthesis. Prolonged hypobaric hypoxia causes placental ER stress, which in turn, moderates protein synthesis and reduces proliferation. Further, Cardiac hypertrophy by cytosolic Ca2+ raises and Ca2+/calmodulin, calcineurin stimulation, NF-AT3 pathway might be caused by an imbalance in Sarcoplasmic reticulum ER Ca2, might be adaptive in beginning but severe later.

scholarly journals Gluconacetobacter diazotrophicus Pal5 Enhances Plant Robustness Status under the Combination of Moderate Drought and Low Nitrogen Stress in Zea mays L.

2021 ◽  
Vol 9 (4) ◽  
pp. 870
Author(s):  
Muhammad Aammar Tufail ◽  
María Touceda-González ◽  
Ilaria Pertot ◽  
Ralf-Udo Ehlers
Keyword(s):  
Zea Mays ◽  
Plant Growth ◽  
Zea Mays L ◽  
Growth Promotion ◽  
Nitrogen Stress ◽  
Rrna Gene ◽  
N Fixation ◽  
Gluconacetobacter Diazotrophicus ◽  
Maize Plants ◽  
Low Nitrogen

Plant growth promoting endophytic bacteria, which can fix nitrogen, plays a vital role in plant growth promotion. Previous authors have evaluated the effect of Gluconacetobacter diazotrophicus Pal5 inoculation on plants subjected to different sources of abiotic stress on an individual basis. The present study aimed to appraise the effect of G. diazotrophicus inoculation on the amelioration of the individual and combined effects of drought and nitrogen stress in maize plants (Zea mays L.). A pot experiment was conducted whereby treatments consisted of maize plants cultivated under drought stress, in soil with a low nitrogen concentration and these two stress sources combined, with and without G. diazotrophicus seed inoculation. The inoculated plants showed increased plant biomass, chlorophyll content, plant nitrogen uptake, and water use efficiency. A general increase in copy numbers of G. diazotrophicus, based on 16S rRNA gene quantification, was detected under combined moderate stress, in addition to an increase in the abundance of genes involved in N fixation (nifH). Endophytic colonization of bacteria was negatively affected by severe stress treatments. Overall, G. diazotrophicus Pal5 can be considered as an effective tool to increase maize crop production under drought conditions with low application of nitrogen fertilizer.

scholarly journals Amino Acid Transporters on the Guard of Cell Genome and Epigenome

Cancers ◽  
2021 ◽  
Vol 13 (1) ◽  
pp. 125
Author(s):  
Uğur Kahya ◽  
Ayşe Sedef Köseer ◽  
Anna Dubrovska
Keyword(s):  
Amino Acid ◽  
Cancer Metabolism ◽  
Tumor Imaging ◽  
Redox Homeostasis ◽  
Amino Acid Uptake ◽  
Metabolic Reprogramming ◽  
Tumor Evolution ◽  
Amino Acid Transporters ◽  
Acid Uptake ◽  
Growth And Survival

Tumorigenesis is driven by metabolic reprogramming. Oncogenic mutations and epigenetic alterations that cause metabolic rewiring may also upregulate the reactive oxygen species (ROS). Precise regulation of the intracellular ROS levels is critical for tumor cell growth and survival. High ROS production leads to the damage of vital macromolecules, such as DNA, proteins, and lipids, causing genomic instability and further tumor evolution. One of the hallmarks of cancer metabolism is deregulated amino acid uptake. In fast-growing tumors, amino acids are not only the source of energy and building intermediates but also critical regulators of redox homeostasis. Amino acid uptake regulates the intracellular glutathione (GSH) levels, endoplasmic reticulum stress, unfolded protein response signaling, mTOR-mediated antioxidant defense, and epigenetic adaptations of tumor cells to oxidative stress. This review summarizes the role of amino acid transporters as the defender of tumor antioxidant system and genome integrity and discusses them as promising therapeutic targets and tumor imaging tools.

scholarly journals Hypoxia, Metabolic Reprogramming, and Drug Resistance in Liver Cancer

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1715
Author(s):  
Macus Hao-Ran Bao ◽  
Carmen Chak-Lui Wong
Keyword(s):  
Hepatocellular Carcinoma ◽  
Drug Resistance ◽  
Liver Cancer ◽  
Effective Treatment ◽  
Molecular Mechanisms ◽  
Hypoxia Inducible Factor ◽  
Metabolic Reprogramming ◽  
Combination Therapies ◽  
Low Oxygen ◽  
Treatment Regimens

Hypoxia, low oxygen (O2) level, is a hallmark of solid cancers, especially hepatocellular carcinoma (HCC), one of the most common and fatal cancers worldwide. Hypoxia contributes to drug resistance in cancer through various molecular mechanisms. In this review, we particularly focus on the roles of hypoxia-inducible factor (HIF)-mediated metabolic reprogramming in drug resistance in HCC. Combination therapies targeting hypoxia-induced metabolic enzymes to overcome drug resistance will also be summarized. Acquisition of drug resistance is the major cause of unsatisfactory clinical outcomes of existing HCC treatments. Extra efforts to identify novel mechanisms to combat refractory hypoxic HCC are warranted for the development of more effective treatment regimens for HCC patients.

scholarly journals Identifying Personalized Metabolic Signatures in Breast Cancer

Metabolites ◽  
2020 ◽  
Vol 11 (1) ◽  
pp. 20
Author(s):  
Priyanka Baloni ◽  
Wikum Dinalankara ◽  
John C. Earls ◽  
Theo A. Knijnenburg ◽  
Donald Geman ◽  
...  
Keyword(s):  
Drug Targets ◽  
Metabolic Networks ◽  
Target Genes ◽  
Enrichment Analysis ◽  
Metabolic Reprogramming ◽  
The Cancer Genome Atlas ◽  
Estrogen Metabolism ◽  
Acid Oxidation ◽  
A Genome ◽  
Context Specific

Cancer cells are adept at reprogramming energy metabolism, and the precise manifestation of this metabolic reprogramming exhibits heterogeneity across individuals (and from cell to cell). In this study, we analyzed the metabolic differences between interpersonal heterogeneous cancer phenotypes. We used divergence analysis on gene expression data of 1156 breast normal and tumor samples from The Cancer Genome Atlas (TCGA) and integrated this information with a genome-scale reconstruction of human metabolism to generate personalized, context-specific metabolic networks. Using this approach, we classified the samples into four distinct groups based on their metabolic profiles. Enrichment analysis of the subsystems indicated that amino acid metabolism, fatty acid oxidation, citric acid cycle, androgen and estrogen metabolism, and reactive oxygen species (ROS) detoxification distinguished these four groups. Additionally, we developed a workflow to identify potential drugs that can selectively target genes associated with the reactions of interest. MG-132 (a proteasome inhibitor) and OSU-03012 (a celecoxib derivative) were the top-ranking drugs identified from our analysis and known to have anti-tumor activity. Our approach has the potential to provide mechanistic insights into cancer-specific metabolic dependencies, ultimately enabling the identification of potential drug targets for each patient independently, contributing to a rational personalized medicine approach.

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