scholarly journals Insect Epigenetic Mechanisms Facing Anthropogenic-Derived Contamination, an Overview

Insects ◽  
2021 ◽  
Vol 12 (9) ◽  
pp. 780
Author(s):  
Gabriela Olivares-Castro ◽  
Lizethly Cáceres-Jensen ◽  
Carlos Guerrero-Bosagna ◽  
Cristian Villagra
Keyword(s):  
Stress Responses ◽  
Molecular Mechanisms ◽  
Chemical Compounds ◽  
Urban Environments ◽  
Human Species ◽  
Compensatory Mechanisms ◽  
Genetic Sequences ◽  
Insect Biology ◽  
Biodiversity Decline ◽  
Soil And Water

Currently, the human species has been recognized as the primary species responsible for Earth’s biodiversity decline. Contamination by different chemical compounds, such as pesticides, is among the main causes of population decreases and species extinction. Insects are key for ecosystem maintenance; unfortunately, their populations are being drastically affected by human-derived disturbances. Pesticides, applied in agricultural and urban environments, are capable of polluting soil and water sources, reaching non-target organisms (native and introduced). Pesticides alter insect’s development, physiology, and inheritance. Recently, a link between pesticide effects on insects and their epigenetic molecular mechanisms (EMMs) has been demonstrated. EMMs are capable of regulating gene expression without modifying genetic sequences, resulting in the expression of different stress responses as well as compensatory mechanisms. In this work, we review the main anthropogenic contaminants capable of affecting insect biology and of triggering EMMs. EMMs are involved in the development of several diseases in native insects affected by pesticides (e.g., anomalous teratogenic reactions). Additionally, EMMs also may allow for the survival of some species (mainly pests) under contamination-derived habitats; this may lead to biodiversity decline and further biotic homogenization. We illustrate these patterns by reviewing the effect of neonicotinoid insecticides, insect EMMs, and their ecological consequences.

scholarly journals Integrated bioinformatics analysis of As, Au, Cd, Pb and Cu heavy metal responsive marker genes through Arabidopsis thaliana GEO datasets

PeerJ ◽  
2019 ◽  
Vol 7 ◽  
pp. e6495 ◽  
Author(s):  
Chao Niu ◽  
Min Jiang ◽  
Na Li ◽  
Jianguo Cao ◽  
Meifang Hou ◽  
...  
Keyword(s):  
Heavy Metals ◽  
Heavy Metal ◽  
Stress Responses ◽  
Large Scale ◽  
Molecular Mechanisms ◽  
Bioinformatics Analysis ◽  
Kegg Pathway ◽  
Marker Genes ◽  
Bioinformatics Analyses ◽  
Soil And Water

Background Current environmental pollution factors, particularly the distribution and diffusion of heavy metals in soil and water, are a high risk to local environments and humans. Despite striking advances in methods to detect contaminants by a variety of chemical and physical solutions, these methods have inherent limitations such as small dimensions and very low coverage. Therefore, identifying novel contaminant biomarkers are urgently needed. Methods To better track heavy metal contaminations in soil and water, integrated bioinformatics analysis to identify biomarkers of relevant heavy metal, such as As, Cd, Pb and Cu, is a suitable method for long-term and large-scale surveys of such heavy metal pollutants. Subsequently, the accuracy and stability of the results screened were experimentally validated by quantitative PCR experiment. Results We obtained 168 differentially expressed genes (DEGs) which contained 59 up-regulated genes and 109 down-regulated genes through comparative bioinformatics analyses. Subsequently, the gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichments of these DEGs were performed, respectively. GO analyses found that these DEGs were mainly related to responses to chemicals, responses to stimulus, responses to stress, responses to abiotic stimulus, and so on. KEGG pathway analyses of DEGs were mainly involved in the protein degradation process and other biologic process, such as the phenylpropanoid biosynthesis pathways and nitrogen metabolism. Moreover, we also speculated that nine candidate core biomarker genes (namely, NILR1, PGPS1, WRKY33, BCS1, AR781, CYP81D8, NR1, EAP1 and MYB15) might be tightly correlated with the response or transport of heavy metals. Finally, experimental results displayed that these genes had the same expression trend response to different stresses as mentioned above (Cd, Pb and Cu) and no mentioned above (Zn and Cr). Conclusion In general, the identified biomarker genes could help us understand the potential molecular mechanisms or signaling pathways responsive to heavy metal stress in plants, and could be applied as marker genes to track heavy metal pollution in soil and water through detecting their expression in plants growing in those environments.

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.

Insights into the molecular basis of host behaviour manipulation by Toxoplasma gondii infection

2017 ◽  
Vol 1 (6) ◽  
pp. 563-572 ◽  
Author(s):  
Pierre-Mehdi Hammoudi ◽  
Dominique Soldati-Favre
Keyword(s):  
Toxoplasma Gondii ◽  
Stress Responses ◽  
Molecular Mechanisms ◽  
Brain Regions ◽  
Intermediate Hosts ◽  
Toxoplasma Gondii Infection ◽  
Host Parasite ◽  
Host Behaviour ◽  
The Brain ◽  
Brain Homeostasis

Typically illustrating the ‘manipulation hypothesis’, Toxoplasma gondii is widely known to trigger sustainable behavioural changes during chronic infection of intermediate hosts to enhance transmission to its feline definitive hosts, ensuring survival and dissemination. During the chronic stage of infection in rodents, a variety of neurological dysfunctions have been unravelled and correlated with the loss of cat fear, among other phenotypic impacts. However, the underlying neurological alteration(s) driving these behavioural modifications is only partially understood, which makes it difficult to draw more than a correlation between T. gondii infection and changes in brain homeostasis. Moreover, it is barely known which among the brain regions governing fear and stress responses are preferentially affected during T. gondii infection. Studies aiming at an in-depth dissection of underlying molecular mechanisms occurring at the host and parasite levels will be discussed in this review. Addressing this reminiscent topic in the light of recent technical progress and new discoveries regarding fear response, olfaction and neuromodulator mechanisms could contribute to a better understanding of this complex host–parasite interaction.

scholarly journals Genome-wide promoter analysis, homology modeling and protein interaction network of Dehydration Responsive Element Binding (DREB) gene family in Solanum tuberosum

PLoS ONE ◽  
2021 ◽  
Vol 16 (12) ◽  
pp. e0261215
Author(s):  
Qurat-ul ain-Ali ◽  
Nida Mushtaq ◽  
Rabia Amir ◽  
Alvina Gul ◽  
Muhammad Tahir ◽  
...  
Keyword(s):  
Abiotic Stress ◽  
Gene Family ◽  
Stress Responses ◽  
Promoter Analysis ◽  
Molecular Mechanisms ◽  
Regulatory Elements ◽  
Start Codon ◽  
Gene Promoters ◽  
Responsive Element ◽  
Dreb Gene

Dehydration Responsive Element Binding (DREB) regulates the expression of numerous stress-responsive genes, and hence plays a pivotal role in abiotic stress responses and tolerance in plants. The study aimed to develop a complete overview of the cis-acting regulatory elements (CAREs) present in S. tuberosum DREB gene promoters. A total of one hundred and four (104) cis-regulatory elements (CREs) were identified from 2.5kbp upstream of the start codon (ATG). The in-silico promoter analysis revealed variable sets of cis-elements and functional diversity with the predominance of light-responsive (30%), development-related (20%), abiotic stress-responsive (14%), and hormone-responsive (12%) elements in StDREBs. Among them, two light-responsive elements (Box-4 and G-box) were predicted in 64 and 61 StDREB genes, respectively. Two development-related motifs (AAGAA-motif and as-1) were abundant in StDREB gene promoters. Most of the DREB genes contained one or more Myeloblastosis (MYB) and Myelocytometosis (MYC) elements associated with abiotic stress responses. Hormone-responsive element i.e. ABRE was found in 59 out of 66 StDREB genes, which implied their role in dehydration and salinity stress. Moreover, six proteins were chosen corresponding to A1-A6 StDREB subgroups for secondary structure analysis and three-dimensional protein modeling followed by model validation through PROCHECK server by Ramachandran Plot. The predicted models demonstrated >90% of the residues in the favorable region, which further ensured their reliability. The present study also anticipated pocket binding sites and disordered regions (DRs) to gain insights into the structural flexibility and functional annotation of StDREB proteins. The protein association network determined the interaction of six selected StDREB proteins with potato proteins encoded by other gene families such as MYB and NAC, suggesting their similar functional roles in biological and molecular pathways. Overall, our results provide fundamental information for future functional analysis to understand the precise molecular mechanisms of the DREB gene family in S. tuberosum.

scholarly journals Altered metal distribution in the sr45-1 Arabidopsis mutant causes developmental defects

2021 ◽  
Author(s):  
Steven Fanara ◽  
Marie Schloesser ◽  
Marc Hanikenne ◽  
Patrick Motte
Keyword(s):  
Stress Responses ◽  
Molecular Mechanisms ◽  
Phenylpropanoid Pathway ◽  
Histochemical Staining ◽  
Metal Distribution ◽  
Iron Starvation ◽  
Developmental Defects ◽  
Developmental Abnormalities ◽  
Arabidopsis Mutant ◽  
Root Tissues

The plant SR (serine/arginine-rich) splicing factor SR45 plays important roles in several biological processes, such as splicing, DNA methylation, innate immunity, glucose regulation and ABA signaling. A homozygous Arabidopsis sr45-1 null mutant is viable, but exhibits diverse phenotypic alterations, including delayed root development, late flowering, shorter siliques with fewer seeds, narrower leaves and petals, and unusual numbers of floral organs. Here, we report that the sr45-1 mutant presents an unexpected constitutive iron deficiency phenotype characterized by altered metal distribution in the plant. RNA-Sequencing highlighted severe perturbations in metal homeostasis, phenylpropanoid pathway, oxidative stress responses, and reproductive development. Ionomic quantification and histochemical staining revealed strong iron accumulation in the sr45-1 root tissues accompanied by an iron starvation in aerial parts. We showed that some sr45-1 developmental abnormalities can be complemented by exogenous iron supply. Our findings provide new insight into the molecular mechanisms governing the phenotypes of the sr45-1 mutant.

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 Overexpression of SgGH3.1 from Fine-Stem Stylo (Stylosanthes guianensis var. intermedia) Enhances Chilling and Cold Tolerance in Arabidopsis thaliana

Genes ◽  
2021 ◽  
Vol 12 (9) ◽  
pp. 1367
Author(s):  
Ming Jiang ◽  
Long-Long Ma ◽  
Huai-An Huang ◽  
Shan-Wen Ke ◽  
Chun-Sheng Gui ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Cold Stress ◽  
Stress Responses ◽  
Molecular Mechanisms ◽  
Transcriptome Profiling ◽  
Pasture Legumes ◽  
Cold Tolerant ◽  
Whole Transcriptome ◽  
Altered Sensitivity ◽  
Exogenous Iaa

Stylosanthes (stylo) species are commercially significant tropical and subtropical forage and pasture legumes that are vulnerable to chilling and frost. However, little is known about the molecular mechanisms behind stylos’ responses to low temperature stress. Gretchen-Hagen 3 (GH3) proteins have been extensively investigated in many plant species for their roles in auxin homeostasis and abiotic stress responses, but none have been reported in stylos. SgGH3.1, a cold-responsive gene identified in a whole transcriptome profiling study of fine-stem stylo (S. guianensis var. intermedia) was further investigated for its involvement in cold stress tolerance. SgGH3.1 shared a high percentage of identity with 14 leguminous GH3 proteins, ranging from 79% to 93%. Phylogenetic analysis classified SgGH3.1 into Group Ⅱ of GH3 family, which have been proven to involve with auxins conjugation. Expression profiling revealed that SgGH3.1 responded rapidly to cold stress in stylo leaves. Overexpression of SgGH3.1 in Arabidopsis thaliana altered sensitivity to exogenous IAA, up-regulated transcription of AtCBF1-3 genes, activated physiological responses against cold stress, and enhanced chilling and cold tolerances. This is the first report of a GH3 gene in stylos, which not only validated its function in IAA homeostasis and cold responses, but also gave insight into breeding of cold-tolerant stylos.

scholarly journals Inhibition of 11β-HSD1 Ameliorates Cognition and Molecular Detrimental Changes after Chronic Mild Stress in SAMP8 Mice

2021 ◽  
Vol 14 (10) ◽  
pp. 1040
Author(s):  
Dolors Puigoriol-Illamola ◽  
Júlia Companys-Alemany ◽  
Kris McGuire ◽  
Natalie Z. M. Homer ◽  
Rosana Leiva ◽  
...  
Keyword(s):  
Stress Responses ◽  
Healthy Aging ◽  
Molecular Mechanisms ◽  
Chronic Mild Stress ◽  
Mild Stress ◽  
Cognitive Improvement ◽  
Age Related ◽  
Mtorc1 Signaling ◽  
Cognitive Disturbances ◽  
Samp8 Mice

Impaired glucocorticoid (GC) signaling is a significant factor in aging, stress, and neurodegenerative diseases such as Alzheimer’s disease. Therefore, the study of GC-mediated stress responses to chronic moderately stressful situations, which occur in daily life, is of huge interest for the design of pharmacological strategies toward the prevention of neurodegeneration. To address this issue, SAMP8 mice were exposed to the chronic mild stress (CMS) paradigm for 4 weeks and treated with RL-118, an 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) inhibitor. The inhibition of this enzyme is linked with a reduction in GC levels and cognitive improvement, while CMS exposure has been associated with reduced cognitive performance. The aim of this project was to assess whether RL-118 treatment could reverse the deleterious effects of CMS on cognition and behavioral abilities and to evaluate the molecular mechanisms that compromise healthy aging in SAMP8 mice. First, we confirmed the target engagement between RL-118 and 11β-HSD1. Additionally, we showed that DNA methylation, hydroxymethylation, and histone phosphorylation were decreased by CMS induction, and increased by RL-118 treatment. In addition, CMS exposure caused the accumulation of reactive oxygen species (ROS)-induced damage and increased pro-oxidant enzymes—as well as pro-inflammatory mediators—through the NF-κB pathway and astrogliosis markers, such as GFAP. Of note, these modifications were reversed by 11β-HSD1 inhibition. Remarkably, although CMS altered mTORC1 signaling, autophagy was increased in the SAMP8 RL-118-treated mice. We also showed an increase in amyloidogenic processes and a decrease in synaptic plasticity and neuronal remodeling markers in mice under CMS, which were consequently modified by RL-118 treatment. In conclusion, 11β-HSD1 inhibition through RL-118 ameliorated the detrimental effects induced by CMS, including epigenetic and cognitive disturbances, indicating that GC-excess attenuation shows potential as a therapeutic strategy for age-related cognitive decline and AD.

Molecular Mechanisms of Listeria monocytogenes Stress Responses

2021 ◽  
pp. 169-186
Author(s):  
Alberto Alía ◽  
Alicia Rodríguez ◽  
María J. Andrade ◽  
Juan J. Córdoba
Keyword(s):  
Listeria Monocytogenes ◽  
Stress Responses ◽  
Molecular Mechanisms

scholarly journals The coupling of translational control and stress responses

2020 ◽  
Vol 168 (2) ◽  
pp. 93-102 ◽  
Author(s):  
Ryan Houston ◽  
Shiori Sekine ◽  
Yusuke Sekine
Keyword(s):  
Stress Response ◽  
Stress Responses ◽  
Translational Control ◽  
Messenger Rna ◽  
Mammalian Cells ◽  
Molecular Mechanisms ◽  
Translation Rate ◽  
Nucleolar Stress ◽  
Multistep Process ◽  
Aminoacyl Transfer

Abstract The translation of messenger RNA (mRNA) into protein is a multistep process by which genetic information transcribed into an mRNA is decoded to produce a specific polypeptide chain of amino acids. Ribosomes play a central role in translation by coordinately working with various translation regulatory factors and aminoacyl-transfer RNAs. Various stresses attenuate the ribosomal synthesis in the nucleolus as well as the translation rate in the cytosol. To efficiently reallocate cellular energy and resources, mammalian cells are endowed with mechanisms that directly link the suppression of translation-related processes to the activation of stress adaptation programmes. This review focuses on the integrated stress response (ISR) and the nucleolar stress response (NSR) both of which are activated by various stressors and selectively upregulate stress-responsive transcription factors. Emerging findings have delineated the detailed molecular mechanisms of the ISR and NSR and expanded their physiological and pathological significances.

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