scholarly journals Primed to be strong, primed to be fast: modeling benefits of microbial stress responses

2019 ◽  
Vol 95 (8) ◽  
Author(s):  
Felix Wesener ◽  
Britta Tietjen

ABSTRACT Organisms are prone to different stressors and have evolved various defense mechanisms. One such defense mechanism is priming, where a mild preceding stress prepares the organism toward an improved stress response. This improved response can strongly vary, and primed organisms have been found to respond with one of three response strategies: a shorter delay to stress, a faster buildup of their response or a more intense response. However, a universal comparative assessment, which response is superior under a given environmental setting, is missing. We investigate the benefits of the three improved responses for microorganisms with an ordinary differential equation model, simulating the impact of an external stress on a microbial population that is either naïve or primed. We systematically assess the resulting population performance for different costs associated with priming and stress conditions. Our results show that independent of stress type and priming costs, the stronger primed response is most beneficial for longer stress phases, while the faster and earlier responses increase population performance and survival probability under short stresses. Competition increases priming benefits and promotes the early stress response. This dependence on the ecological context highlights the importance of including primed response strategies into microbial stress ecology.

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Ning Li ◽  
Suzana Stojanovski ◽  
Pierre Maechler

In pancreaticβcells, mitochondrial metabolism translates glucose sensing into signals regulating insulin secretion. Chronic exposure ofβcells to excessive nutrients, namely, glucolipotoxicity, impairsβ-cell function. This is associated with elevated ROS production from overstimulated mitochondria. Mitochondria are not only the major source of cellular ROS, they are also the primary target of ROS attacks. The mitochondrial uncoupling protein UCP2, even though its uncoupling properties are debated, has been associated with protective functions against ROS toxicity. Hormesis, an adaptive response to cellular stresses, might contribute to the protection againstβ-cell death, possibly limiting the development of type 2 diabetes. Mitochondrial hormesis, or mitohormesis, is a defense mechanism observed in ROS-induced stress-responses by mitochondria. Inβcells, mitochondrial damages induced by sublethal exogenous H2O2can induce secondary repair and defense mechanisms. In this context, UCP2 is a marker of mitohormesis, being upregulated following stress conditions. When overexpressed in nonstressed naïve cells, UCP2 confers resistance to oxidative stress. Whether treatment with mitohormetic inducers is sufficient to restore or ameliorate secretory function ofβcells remains to be determined.


Plants ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1733
Author(s):  
Ho Viet Khoa ◽  
Puja Kumari ◽  
Hiroko Uchida ◽  
Akio Murakami ◽  
Satoshi Shimada ◽  
...  

The red alga ‘Bangia’ sp. ESS1, a ‘Bangia’ 2 clade member, responds to heat stress via accelerated asexual reproduction and acquires thermotolerance based on heat-stress memory. However, whether these strategies are specific to ‘Bangia’ 2, especially ‘Bangia’ sp. ESS1, or whether they are employed by all ‘Bangia’ species is currently unknown. Here, we examined the heat-stress responses of ‘Bangia’ sp. ESS2, a newly identified ‘Bangia’ clade 3 member, and Bangia atropurpurea. Intrinsic thermotolerance differed among species: Whereas ‘Bangia’ sp. ESS1 survived at 30 °C for 7 days, ‘Bangia’ sp. ESS2 and B. atropurpurea did not, with B. atropurpurea showing the highest heat sensitivity. Under sublethal heat stress, the release of asexual spores was highly repressed in ‘Bangia’ sp. ESS2 and completely repressed in B. atropurpurea, whereas it was enhanced in ‘Bangia’ sp. ESS1. ‘Bangia’ sp. ESS2 failed to acquire heat-stress tolerance under sublethal heat-stress conditions, whereas the acquisition of heat tolerance by priming with sublethal high temperatures was observed in both B. atropurpurea and ‘Bangia’ sp. ESS1. Finally, unlike ‘Bangia’ sp. ESS1, neither ‘Bangia’ sp. ESS2 nor B. atropurpurea acquired heat-stress memory. These findings provide insights into the diverse heat-stress response strategies among species from different clades of ‘Bangia’.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. 667-667
Author(s):  
Bradford Hull ◽  
George Sutphin

Abstract Cellular stress is a fundamental component of age-associated disease. Cells experience many forms of stress (oxidative, heavy metal, etc.), and as we age the burden of stress and resulting damage increases while our cells’ ability to deal with the consequences becomes diminished due to dysregulation of cellular stress response pathways. By understanding how cells respond to stress we aim to slow age-associated deterioration and develop treatment targets for age-associated disease. The majority of past work has focused on understanding responses to individual stressors. In contrast, how pathology and stress responses differ in the presence of multiple stressors is relatively unknown; we investigate that here. We cultured worms on agar plates with different combinations of arsenic, copper, and DTT (which create oxidative/proteotoxic, heavy metal, and endoplasmic reticulum (ER) stress, respectively) at doses that result in 20% lifespan reduction individually and measured the effect on lifespan. We found that arsenic/copper and arsenic/DTT combinations created additive lifespan reductions while the copper/DTT combination created an antagonistic lifespan reduction when compared to controls (p<0.05). This antagonistic toxicity suggests an interaction either between the mechanisms of toxicity or the cellular response to copper and DTT. We are now evaluating the impact of copper and DTT individually and in combination on unfolded protein and heavy metal response pathways to understand the underlying mechanism of the interaction. Additionally, we are continuing to screen stressors to identify combinations that cause non-additive (synergistic or antagonistic) toxicity to build a comprehensive model of the genetic stress response network in C. elegans.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Mercedes Viettri ◽  
José L. Zambrano ◽  
Romel Rosales ◽  
Gerson I. Caraballo ◽  
Ana Lorena Gutiérrez-Escolano ◽  
...  

AbstractThe stress of the Golgi apparatus is an autoregulatory mechanism that is induced to compensate for greater demand in the Golgi functions. No examples of Golgi stress responses due to physiological stimuli are known. Furthermore, the impact on this organelle of viral infections that occupy the vesicular transport during replication is unknown. In this work, we evaluated if a Golgi stress response is triggered during dengue and Zika viruses replication, two flaviviruses whose replicative cycle is heavily involved with the Golgi complex, in vertebrate and mosquito cells. Using GM-130 as a Golgi marker, and treatment with monensin as a positive control for the induction of the Golgi stress response, a significant expansion of the Golgi cisternae was observed in BHK-21, Vero E6 and mosquito cells infected with either virus. Activation of the TFE3 pathway was observed in the infected cells as indicated by the translocation from the cytoplasm to the nucleus of TFE3 and increased expression of pathway targeted genes. Of note, no sign of activation of the stress response was observed in CRFK cells infected with Feline Calicivirus (FCV), a virus released by cell lysis, not requiring vesicular transport. Finally, dilatation of the Golgi complex and translocation of TFE3 was observed in vertebrate cells expressing dengue and Zika viruses NS1, but not NS3. These results indicated that infections by dengue and Zika viruses induce a Golgi stress response in vertebrate and mosquito cells due to the increased demand on the Golgi complex imposed by virion and NS1 processing and secretion.


2021 ◽  
Vol 12 ◽  
Author(s):  
Zahra Iqbal ◽  
Mohammed Shariq Iqbal ◽  
Abeer Hashem ◽  
Elsayed Fathi Abd_Allah ◽  
Mohammad Israil Ansari

Plants are subjected to a plethora of environmental cues that cause extreme losses to crop productivity. Due to fluctuating environmental conditions, plants encounter difficulties in attaining full genetic potential for growth and reproduction. One such environmental condition is the recurrent attack on plants by herbivores and microbial pathogens. To surmount such attacks, plants have developed a complex array of defense mechanisms. The defense mechanism can be either preformed, where toxic secondary metabolites are stored; or can be inducible, where defense is activated upon detection of an attack. Plants sense biotic stress conditions, activate the regulatory or transcriptional machinery, and eventually generate an appropriate response. Plant defense against pathogen attack is well understood, but the interplay and impact of different signals to generate defense responses against biotic stress still remain elusive. The impact of light and dark signals on biotic stress response is one such area to comprehend. Light and dark alterations not only regulate defense mechanisms impacting plant development and biochemistry but also bestow resistance against invading pathogens. The interaction between plant defense and dark/light environment activates a signaling cascade. This signaling cascade acts as a connecting link between perception of biotic stress, dark/light environment, and generation of an appropriate physiological or biochemical response. The present review highlights molecular responses arising from dark/light fluctuations vis-à-vis elicitation of defense mechanisms in plants.


2021 ◽  
Author(s):  
Mercedes Viettri ◽  
José L. Zambrano ◽  
Romel Rosales-Ramirez ◽  
Ana Lorena Gutierrez-Escolano ◽  
Juan E Ludert

Abstract The stress of the Golgi apparatus is an autoregulatory mechanism that is induced to compensate for greater demand in the Golgi functions. Few examples of Golgi stress responses due to physiological stimuli are known. Furthermore, the impact on this organelle of viral infections that occupy the vesicular transport during replication is unknown. In this work, we evaluated if a Golgi stress response is triggered during dengue and Zika viruses replication, two flaviviruses whose replicative cycle is heavily involved with the Golgi complex, in vertebrate and mosquito cells. Using GM-130 as a Golgi marker, and treatment with monensin as a positive control for the induction of the Golgi stress response, a significant expansion of the Golgi cisternae was observed in BHK-21, Vero E6 and mosquito cells infected with either virus. Activation of the TFE3 pathway was observed in the infected cells as indicated by the translocation from the cytoplasm to the nucleus of TFE3. Of note, no sign of activation of the stress response was observed in CRFK cells infected with Feline Calicivirus (FCV), a virus released by cell lysis, not requiring vesicular transport. Finally, dilatation of the Golgi complex and translocation of TFE3 was observed in vertebrate cells expressing dengue and Zika viruses NS1, but not NS3. These results indicated that infections by dengue and Zika viruses induce a Golgi stress response in vertebrate and mosquito cells due to the increased demand on Golgi complex imposed by virion and NS1 processing and secretion.


2005 ◽  
Vol 289 (3) ◽  
pp. R738-R744 ◽  
Author(s):  
Firdaus S. Dhabhar ◽  
Kavitha Viswanathan

It would be extremely beneficial if one could harness natural, endogenous, health-promoting defense mechanisms to fight disease and restore health. The psychophysiological stress response is the most underappreciated of nature's survival mechanisms. We show that acute stress experienced before primary immunization induces a long-lasting increase in immunity. Compared with controls, mice restrained for 2.5 h before primary immunization with keyhole limpet hemocyanin (KLH) show a significantly enhanced immune response when reexposed to KLH 9 mo later. This immunoenhancement is mediated by an increase in numbers of memory and effector helper T cells in sentinel lymph nodes at the time of primary immunization. Further analyses show that the early stress-induced increase in T cell memory may stimulate the robust increase in infiltrating lymphocyte and macrophage numbers observed months later at a novel site of antigen reexposure. Enhanced leukocyte infiltration may be driven by increased levels of the type 1 cytokines, IL-2 and IFN-γ, and TNF-α, observed at the site of antigen reexposure in animals that had been stressed at the time of primary immunization. In contrast, no differences were observed in type 2 cytokines, IL-4 or IL-5. Given the importance of inducing long-lasting increases in immunologic memory during vaccination, we suggest that the neuroendocrine stress response is nature's adjuvant that could be psychologically and/or pharmacologically manipulated to safely increase vaccine efficacy. These studies introduce the novel concept that a psychophysiological stress response is nature's fundamental survival mechanism that could be therapeutically harnessed to augment immune function during vaccination, wound healing, or infection.


Author(s):  
Rebeen Rebwar Hama Amin ◽  
Dana Hassan ◽  
Masnida Hussin

DNS reflection/amplification attacks are types of Distributed Denial of Service (DDoS) attacks that take advantage of vulnerabilities in the Domain Name System (DNS) and use it as an attacking tool. This type of attack can quickly deplete the resources (i.e. computational and bandwidth) of the targeted system. Many defense mechanisms are proposed to mitigate the impact of this type of attack. However, these defense mechanisms are centralized-based and cannot deal with a distributed-based attack. Also, these defense mechanisms have a single point of deployment which leads to a lack of computational resources to handle an attack with a large magnitude. In this work, we presented a new distributed-based defense mechanism (DDM) to counter reflection/ amplification attacks. While operating, we calculated the CPU counters of the machines that we deployed our defense mechanism with which showed 19.9% computational improvement. On top of that, our defense mechanism showed that it can protect the attack path from exhaustion during reflection/amplification attacks without putting any significant traffic load on the network by eliminating every spoofed request from getting responses.


2019 ◽  
Author(s):  
Yang Liu ◽  
Shuai Liu ◽  
Yanwu Deng ◽  
Chenjiang You ◽  
Weixin Zhang ◽  
...  

Abstract Background One of the main pathways for cadmium (Cd) transfer from the environment to the human body is through the consumption of leafy vegetables, and Brassica leafy crops tend to be Cd hyper-accumulators. But its response strategies to Cd still lack of systematic study. Results To investigate Brassica response strategies to Cd, we identified two cultivars with different Cd translocation efficiencies and performed mutli-transcriptomic sequencing studies under Cd treatments. Certain transporter families exhibited different temporal expression profiles in the two cultivars and may underlie the different Cd translocation efficiencies. Cd induced a drastic reduction of a 22 nt small RNA, the footprint of a pentatricopeptide repeat (PPR) protein on the chloroplast ndhB transcript and the concomitant down-regulation of the ndhB transcript. A global reduction in the expression of PPR genes was found, revealing previously unknown effects of Cd on organellar gene expression. Analyses of microRNAs (miRNAs) and their target genes by small RNA and degradome sequencing not only revealed Cd-induced changes in miRNAs but also implicated the existence of a regulatory cascade involving bra-miR156, its target gene, and bra-miR397 and bra-miR398 in Cd stress responses. Conclusions The present findings help uncover the impact of Cd stress on the transcriptome of B. parachinensis and provide candidate genes and miRNAs for further investigation.


2020 ◽  
Vol 1 ◽  
pp. 6
Author(s):  
Petru Hlihor ◽  
Riccardo Volpi ◽  
Luigi Malagò

Adversarial Examples represent a serious problem affecting the security of machine learning systems. In this paper we focus on a defense mechanism based on reconstructing images before classification using an autoencoder. We experiment on several types of autoencoders and evaluate the impact of strategies such as injecting noise in the input during training and in the latent space at inference time.We tested the models on adversarial examples generated with the Carlini-Wagner attack, in a white-box scenario and on the stacked system composed by the autoencoder and the classifier.


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