scholarly journals An ATP- and hsc70-dependent oligomerization of nascent heat-shock factor (HSF) polypeptide suggests that HSF itself could be a “sensor” for the cellular stress response

1993 ◽  
Vol 2 (8) ◽  
pp. 1356-1360 ◽  
Author(s):  
Milton J. Schlesinger ◽  
Christine Ryan
Keyword(s):  
Stress Response ◽  
Heat Shock ◽  
Cellular Stress ◽  
Heat Shock Factor ◽  
Cellular Stress Response

scholarly journals The cellular stress response of rat skeletal muscle following lengthening contractions

2017 ◽  
Vol 42 (7) ◽  
pp. 708-715 ◽  
Author(s):  
Evan Pollock-Tahiri ◽  
Marius Locke
Keyword(s):  
Stress Response ◽  
Heat Shock ◽  
Muscle Fibre ◽  
Cellular Stress ◽  
Cellular Stress Response ◽  
In Vivo Model ◽  
Morphological Evidence ◽  
Lengthening Contractions ◽  
Single Set

The cellular stress response of the rat tibialis anterior (TA) muscle was investigated following 20, 40, or 60 lengthening contractions (LCs) using an in vivo model of electrical stimulation. Muscles were removed at 0, 1, 3, or 24 h after LCs and assessed for heat shock transcription factor (HSF) activation, heat shock protein (HSP) content, and/or morphological evidence of muscle fibre damage. When compared with the first muscle contraction, peak muscle torque was reduced by 26% (p < 0.05) after 20 LCs and further reduced to 56% and 60% (p < 0.001) after 40 and 60 LCs, respectively. Following 60 LCs, HSF activation was detected at 0, 1, and 3 h but was undetectable at 24 h. Hsp72 content was elevated at 24 h after 20 LCs (2.34 ± 0.37 fold, p < 0.05), 40 LCs (3.02 ± 0.31 fold, p < 0.01), and 60 LCs (3.37 ± 0.21 fold, p < 0.001). Hsp25 content increased after 40 (2.36 ± 0.24 fold, p < 0.01) and 60 LCs (2.80 ± 0.37 fold, p < 0.01). Morphological assessment of TA morphology revealed that very few fibres were damaged following 20 LCs while multiple sets of LCs (40 and 60) caused greater amounts of fibre damage. Electron microscopy showed disrupted Z-lines and sarcomeres were detectable in some muscles fibres following 20 LCs but were more prevalent and severe in muscles subjected to 40 or 60 LCs. These results suggest LCs elevate HSP content by an HSF-mediated mechanism (60 LC) and a single set of 20 LCs is capable of increasing muscle HSP content without causing significant muscle fibre damage.

scholarly journals Flavonoids: Potential Candidates for the Treatment of Neurodegenerative Disorders

Biomedicines ◽  
2021 ◽  
Vol 9 (2) ◽  
pp. 99
Author(s):  
Shweta Devi ◽  
Vijay Kumar ◽  
Sandeep Kumar Singh ◽  
Ashish Kant Dubey ◽  
Jong-Joo Kim
Keyword(s):  
Stress Response ◽  
Stress Responses ◽  
Neurodegenerative Disorders ◽  
Cell Damage ◽  
Cellular Stress ◽  
Clinical Manifestations ◽  
Cellular Stress Response ◽  
Dramatic Rise ◽  
Cellular Stress Responses

Neurodegenerative disorders, such as Parkinson’s disease (PD), Alzheimer’s disease (AD), Amyotrophic lateral sclerosis (ALS), and Huntington’s disease (HD), are the most concerning disorders due to the lack of effective therapy and dramatic rise in affected cases. Although these disorders have diverse clinical manifestations, they all share a common cellular stress response. These cellular stress responses including neuroinflammation, oxidative stress, proteotoxicity, and endoplasmic reticulum (ER)-stress, which combats with stress conditions. Environmental stress/toxicity weakened the cellular stress response which results in cell damage. Small molecules, such as flavonoids, could reduce cellular stress and have gained much attention in recent years. Evidence has shown the potential use of flavonoids in several ways, such as antioxidants, anti-inflammatory, and anti-apoptotic, yet their mechanism is still elusive. This review provides an insight into the potential role of flavonoids against cellular stress response that prevent the pathogenesis of neurodegenerative disorders.

scholarly journals Mitochondrien unter Stress: Die Rolle der Präsequenzprotease MPP

BIOspektrum ◽  
2021 ◽  
Vol 27 (4) ◽  
pp. 390-393
Author(s):  
F.-Nora Vögtle
Keyword(s):  
Stress Response ◽  
Cellular Stress ◽  
Critical Role ◽  
Mitochondrial Protein ◽  
Nuclear Genome ◽  
Cellular Stress Response ◽  
Mitochondrial Proteins ◽  
Protein Biogenesis ◽  
Cellular Integrity

AbstractThe majority of mitochondrial proteins are encoded in the nuclear genome, so that the nearly entire proteome is assembled by post-translational preprotein import from the cytosol. Proteomic imbalances are sensed and induce cellular stress response pathways to restore proteostasis. Here, the mitochondrial presequence protease MPP serves as example to illustrate the critical role of mitochondrial protein biogenesis and proteostasis on cellular integrity.

scholarly journals m5U54 tRNA Hypomodification by Lack of TRMT2A Drives the Generation of tRNA-Derived Small RNAs

2021 ◽  
Vol 22 (6) ◽  
pp. 2941
Author(s):  
Marisa Pereira ◽  
Diana R. Ribeiro ◽  
Miguel M. Pinheiro ◽  
Margarida Ferreira ◽  
Stefanie Kellner ◽  
...  
Keyword(s):  
Stress Response ◽  
Small Rnas ◽  
Mammalian Cells ◽  
Cellular Stress ◽  
Cellular Stress Response ◽  
Translation Regulation ◽  
Translation Efficiency ◽  
Down Regulation ◽  
Gene Expression Control ◽  
The Impact

Transfer RNA (tRNA) molecules contain various post-transcriptional modifications that are crucial for tRNA stability, translation efficiency, and fidelity. Besides their canonical roles in translation, tRNAs also originate tRNA-derived small RNAs (tsRNAs), a class of small non-coding RNAs with regulatory functions ranging from translation regulation to gene expression control and cellular stress response. Recent evidence indicates that tsRNAs are also modified, however, the impact of tRNA epitranscriptome deregulation on tsRNAs generation is only now beginning to be uncovered. The 5-methyluridine (m5U) modification at position 54 of cytosolic tRNAs is one of the most common and conserved tRNA modifications among species. The tRNA methyltransferase TRMT2A catalyzes this modification, but its biological role remains mostly unexplored. Here, we show that TRMT2A knockdown in human cells induces m5U54 tRNA hypomodification and tsRNA formation. More specifically, m5U54 hypomodification is followed by overexpression of the ribonuclease angiogenin (ANG) that cleaves tRNAs near the anticodon, resulting in accumulation of 5′tRNA-derived stress-induced RNAs (5′tiRNAs), namely 5′tiRNA-GlyGCC and 5′tiRNA-GluCTC, among others. Additionally, transcriptomic analysis confirms that down-regulation of TRMT2A and consequently m5U54 hypomodification impacts the cellular stress response and RNA stability, which is often correlated with tiRNA generation. Accordingly, exposure to oxidative stress conditions induces TRMT2A down-regulation and tiRNA formation in mammalian cells. These results establish a link between tRNA hypomethylation and ANG-dependent tsRNAs formation and unravel m5U54 as a tRNA cleavage protective mark.

scholarly journals C. elegans discriminates colors to guide foraging

Science ◽  
2021 ◽  
Vol 371 (6533) ◽  
pp. 1059-1063 ◽  
Author(s):  
D. Dipon Ghosh ◽  
Dongyeop Lee ◽  
Xin Jin ◽  
H. Robert Horvitz ◽  
Michael N. Nitabach
Keyword(s):  
Stress Response ◽  
Cellular Stress ◽  
Color Discrimination ◽  
Cellular Stress Response ◽  
Blue Pigment ◽  
Natural Environments ◽  
C Elegans ◽  
Evolutionarily Conserved ◽  
Foraging Decisions ◽  
Light Guides

Color detection is used by animals of diverse phyla to navigate colorful natural environments and is thought to require evolutionarily conserved opsin photoreceptor genes. We report that Caenorhabditis elegans roundworms can discriminate between colors despite the fact that they lack eyes and opsins. Specifically, we found that white light guides C. elegans foraging decisions away from a blue-pigment toxin secreted by harmful bacteria. These foraging decisions are guided by specific blue-to-amber ratios of light. The color specificity of color-dependent foraging varies notably among wild C. elegans strains, which indicates that color discrimination is ecologically important. We identified two evolutionarily conserved cellular stress response genes required for opsin-independent, color-dependent foraging by C. elegans, and we speculate that cellular stress response pathways can mediate spectral discrimination by photosensitive cells and organisms—even by those lacking opsins.

scholarly journals Induction and transmission of oncogene-induced senescence

2020 ◽  
Author(s):  
Nattaphong Rattanavirotkul ◽  
Kristina Kirschner ◽  
Tamir Chandra
Keyword(s):  
Stress Response ◽  
Single Cell ◽  
Cellular Stress ◽  
Cellular Stress Response ◽  
End Points ◽  
Oncogene Activation ◽  
Suppressor Mechanism ◽  
Bona Fide ◽  
Organ Level ◽  
Complex Scenario

Abstract Senescence is a cellular stress response triggered by diverse stressors, including oncogene activation, where it serves as a bona-fide tumour suppressor mechanism. Senescence can be transmitted to neighbouring cells, known as paracrine secondary senescence. Secondary senescence was initially described as a paracrine mechanism, but recent evidence suggests a more complex scenario involving juxtacrine communication between cells. In addition, single-cell studies described differences between primary and secondary senescent end-points, which have thus far not been considered functionally distinct. Here we discuss emerging concepts in senescence transmission and heterogeneity in primary and secondary senescence on a cellular and organ level.

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