Role of the glutathione/glutaredoxin and thioredoxin systems in yeast growth and response to stress conditions

The Lon protein is a protease implicated in the virulence of many pathogenic bacteria, including some plant pathogens. However, little is known about the role of Lon in bacteria from genus Dickeya. This group of bacteria includes important potato pathogens, with the most aggressive species, D. solani. To determine the importance of Lon for pathogenicity and response to stress conditions of bacteria, we constructed a D. solani Δlon strain. The mutant bacteria showed increased sensitivity to certain stress conditions, in particular osmotic and high-temperature stresses. Furthermore, qPCR analysis showed an increased expression of the lon gene in D. solani under these conditions. The deletion of the lon gene resulted in decreased motility, lower activity of secreted pectinolytic enzymes and finally delayed onset of blackleg symptoms in the potato plants. In the Δlon cells, the altered levels of several proteins, including virulence factors and proteins associated with virulence, were detected by means of Sequential Window Acquisition of All Theoretical Mass Spectra (SWATH-MS) analysis. These included components of the type III secretion system and proteins involved in bacterial motility. Our results indicate that Lon protease is important for D. solani to withstand stressful conditions and effectively invade the potato plant.

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Impact of Hydrogen Peroxide on Protein Synthesis in Yeast

Antioxidants ◽

10.3390/antiox10060952 ◽

2021 ◽

Vol 10 (6) ◽

pp. 952

Author(s):

Cecilia Picazo ◽

Mikael Molin

Keyword(s):

Hydrogen Peroxide ◽

Protein Synthesis ◽

Normal Function ◽

Stress Conditions ◽

Antioxidant Systems ◽

Translation Process ◽

Response To Stress ◽

Accumulation Of Damage ◽

Expensive Process

Cells must be able to respond and adapt to different stress conditions to maintain normal function. A common response to stress is the global inhibition of protein synthesis. Protein synthesis is an expensive process consuming much of the cell’s energy. Consequently, it must be tightly regulated to conserve resources. One of these stress conditions is oxidative stress, resulting from the accumulation of reactive oxygen species (ROS) mainly produced by the mitochondria but also by other intracellular sources. Cells utilize a variety of antioxidant systems to protect against ROS, directing signaling and adaptation responses at lower levels and/or detoxification as levels increase to preclude the accumulation of damage. In this review, we focus on the role of hydrogen peroxide, H2O2, as a signaling molecule regulating protein synthesis at different levels, including transcription and various parts of the translation process, e.g., initiation, elongation, termination and ribosome recycling.

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The Role of Phyto-Melatonin and Related Metabolites in Response to Stress

Molecules ◽

10.3390/molecules23081887 ◽

2018 ◽

Vol 23 (8) ◽

pp. 1887 ◽

Cited By ~ 27

Author(s):

Yang Yu ◽

Yan Lv ◽

Yana Shi ◽

Tao Li ◽

Yanchun Chen ◽

...

Keyword(s):

Stress Tolerance ◽

Metabolic Pathways ◽

Plant Stress ◽

Stress Conditions ◽

Photosynthesis Inhibition ◽

Response To Stress ◽

Plant Stress Tolerance ◽

New Perspective ◽

Catabolism Pathway

Plant hormone candidate melatonin has been widely studied in plants under various stress conditions, such as heat, cold, salt, drought, heavy metal, and pathogen attack. Under stress, melatonin usually accumulates sharply by modulating its biosynthesis and metabolic pathways. Beginning from the precursor tryptophan, four consecutive enzymes mediate the biosynthesis of tryptamine or 5-hydroxytryptophan, serotonin, N-acetylserotonin or 5-methoxytryptamine, and melatonin. Then, the compound is catabolized into 2-hydroxymelatonin, cyclic-3-hydroxymelatonin, and N1-acetyl-N2-formyl-5-methoxyknuramine through 2-oxoglutarate-dependent dioxygenase catalysis or reaction with reactive oxygen species. As an ancient and powerful antioxidant, melatonin directly scavenges ROS induced by various stress conditions. Furthermore, it confreres stress tolerance by activating the plant’s antioxidant system, alleviating photosynthesis inhibition, modulating transcription factors that are involved with stress resisting, and chelating and promoting the transport of heavy metals. Melatonin is even proven to defense against pathogen attacks for the plant by activating other stress-relevant hormones, like salicylic acid, ethylene, and jasmonic acid. Intriguingly, other precursors and metabolite molecules involved with melatonin also can increase stress tolerance for plant except for unconfirmed 5-methoxytryptamine, cyclic-3-hydroxymelatonin, and N1-acetyl-N2-formyl-5-methoxyknuramine. Therefore, the precursors and metabolites locating at the whole biosynthesis and catabolism pathway of melatonin could contribute to plant stress resistance, thus providing a new perspective for promoting plant stress tolerance.

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HigB1 Toxin in Mycobacterium tuberculosis Is Upregulated During Stress and Required to Establish Infection in Guinea Pigs

Frontiers in Microbiology ◽

10.3389/fmicb.2021.748890 ◽

2021 ◽

Vol 12 ◽

Author(s):

Arun Sharma ◽

Kalpana Sagar ◽

Neeraj Kumar Chauhan ◽

Balaji Venkataraman ◽

Nidhi Gupta ◽

...

Keyword(s):

Mycobacterium Tuberculosis ◽

Guinea Pigs ◽

Physiological Role ◽

Stress Conditions ◽

Expression Of Genes ◽

Response To Stress ◽

Cumulative Evidence ◽

Host Tissues

The extraordinary expansion of Toxin Antitoxin (TA) modules in the genome of Mycobacterium tuberculosis has received significant attention over the last few decades. The cumulative evidence suggests that TA systems are activated in response to stress conditions and are essential for M. tuberculosis pathogenesis. In M. tuberculosis, Rv1955-Rv1956-Rv1957 constitutes the only tripartite TAC (Toxin Antitoxin Chaperone) module. In this locus, Rv1955 (HigB1) encodes for the toxin and Rv1956 (HigA1) encodes for antitoxin. Rv1957 encodes for a SecB-like chaperone that regulates HigBA1 toxin antitoxin system by preventing HigA1 degradation. Here, we have investigated the physiological role of HigB1 toxin in stress adaptation and pathogenesis of Mycobacterium tuberculosis. qPCR studies revealed that higBA1 is upregulated in nutrient limiting conditions and upon exposure to levofloxacin. We also show that the promoter activity of higBA1 locus in M. tuberculosis is (p)ppGpp dependent. We observed that HigB1 locus is non-essential for M. tuberculosis growth under different stress conditions in vitro. However, guinea pigs infected with higB1 deletion strain exhibited significantly reduced bacterial loads and pathological damage in comparison to the animals infected with the parental strain. Transcriptome analysis suggested that deletion of higB1 reduced the expression of genes involved in virulence, detoxification and adaptation. The present study describes the role of higB1 toxin in M. tuberculosis physiology and highlights the importance of higBA1 locus during infection in host tissues.

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A Conserved Stress-activated Protein Kinase Regulates a Core Stress Response in the Human PathogenCandida albicans

Molecular Biology of the Cell ◽

10.1091/mbc.e04-03-0181 ◽

2004 ◽

Vol 15 (9) ◽

pp. 4179-4190 ◽

Cited By ~ 200

Author(s):

Deborah A. Smith ◽

Susan Nicholls ◽

Brian A. Morgan ◽

Alistair J.P. Brown ◽

Janet Quinn

Keyword(s):

Stress Response ◽

Protein Kinase ◽

Stress Responses ◽

Stress Conditions ◽

Human Pathogen ◽

Environmental Niche ◽

The Core ◽

Response To Stress ◽

Molecular Circuitry

Previous work has implicated the Hog1 stress-activated protein kinase (SAPK) in osmotic and oxidative stress responses in the human pathogen Candida albicans. In this study, we have characterized the role of Hog1 in mediating these and other stress responses in C. albicans. We provide evidence that a SAPK-dependent core stress response exists in this pathogen. The Hog1 SAPK is phosphorylated and it accumulates in the nucleus in response to diverse stress conditions. In addition, we have identified Hog1-regulated genes that are induced in response to stress conditions that activate Hog1. These analyses reveal both activator and repressor functions for the Hog1 SAPK. Our results also demonstrate that stress cross-protection, a classical hallmark of the core stress response, occurs in C. albicans between stresses that activate the Hog1 SAPK. Importantly, we find that the core stress response in C. albicans has adapted to the environmental niche of this human pathogen. This niche specificity is reflected by the specific environmental conditions that drive the Hog1-regulated core stress response in C. albicans and by differences in the molecular circuitry that control this response.

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Support seeking in response to stress: Person-level moderators, contextual factors, and the role of online venues

PsycEXTRA Dataset ◽

10.1037/e578192014-944 ◽

2014 ◽

Cited By ~ 1

Author(s):

Sean Chandler Rife ◽

Kathryn A. Kerns ◽

John A. Updegraff

Keyword(s):

Contextual Factors ◽

Response To Stress ◽

Support Seeking

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Selectivity of mRNA degradation by autophagy in yeast

Nature Communications ◽

10.1038/s41467-021-22574-6 ◽

2021 ◽

Vol 12 (1) ◽

Author(s):

Shiho Makino ◽

Tomoko Kawamata ◽

Shintaro Iwasaki ◽

Yoshinori Ohsumi

Keyword(s):

Ribosomal Proteins ◽

Rna Degradation ◽

Mrna Degradation ◽

Ribosome Profiling ◽

Genome Wide ◽

Tightly Coupled ◽

Response To Stress ◽

Transcriptional Gene Regulation ◽

Synthesis And Degradation

AbstractSynthesis and degradation of cellular constituents must be balanced to maintain cellular homeostasis, especially during adaptation to environmental stress. The role of autophagy in the degradation of proteins and organelles is well-characterized. However, autophagy-mediated RNA degradation in response to stress and the potential preference of specific RNAs to undergo autophagy-mediated degradation have not been examined. In this study, we demonstrate selective mRNA degradation by rapamycin-induced autophagy in yeast. Profiling of mRNAs from the vacuole reveals that subsets of mRNAs, such as those encoding amino acid biosynthesis and ribosomal proteins, are preferentially delivered to the vacuole by autophagy for degradation. We also reveal that autophagy-mediated mRNA degradation is tightly coupled with translation by ribosomes. Genome-wide ribosome profiling suggested a high correspondence between ribosome association and targeting to the vacuole. We propose that autophagy-mediated mRNA degradation is a unique and previously-unappreciated function of autophagy that affords post-transcriptional gene regulation.

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Impaired eIF5A function causes a Mendelian disorder that is partially rescued in model systems by spermidine

Nature Communications ◽

10.1038/s41467-021-21053-2 ◽

2021 ◽

Vol 12 (1) ◽

Author(s):

Víctor Faundes ◽

Martin D. Jennings ◽

Siobhan Crilly ◽

Sarah Legraie ◽

Sarah E. Withers ◽

...

Keyword(s):

De Novo ◽

Model Systems ◽

Yeast Growth ◽

Related Disorder ◽

Optimal Position ◽

Human Phenotype ◽

Mendelian Disorder ◽

Growth Defects ◽

Polysome Profiling

AbstractThe structure of proline prevents it from adopting an optimal position for rapid protein synthesis. Poly-proline-tract (PPT) associated ribosomal stalling is resolved by highly conserved eIF5A, the only protein to contain the amino acid hypusine. We show that de novo heterozygous EIF5A variants cause a disorder characterized by variable combinations of developmental delay, microcephaly, micrognathia and dysmorphism. Yeast growth assays, polysome profiling, total/hypusinated eIF5A levels and PPT-reporters studies reveal that the variants impair eIF5A function, reduce eIF5A-ribosome interactions and impair the synthesis of PPT-containing proteins. Supplementation with 1 mM spermidine partially corrects the yeast growth defects, improves the polysome profiles and restores expression of PPT reporters. In zebrafish, knockdown eif5a partly recapitulates the human phenotype that can be rescued with 1 µM spermidine supplementation. In summary, we uncover the role of eIF5A in human development and disease, demonstrate the mechanistic complexity of EIF5A-related disorder and raise possibilities for its treatment.

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