C. elegans discriminates colors to guide foraging

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.

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Effect of Combined Stressors on C. elegans Lifespan

Innovation in Aging ◽

10.1093/geroni/igab046.2499 ◽

2021 ◽

Vol 5 (Supplement_1) ◽

pp. 667-667

Author(s):

Bradford Hull ◽

George Sutphin

Keyword(s):

Heavy Metal ◽

Stress Response ◽

Stress Responses ◽

Cellular Response ◽

Multiple Stressors ◽

Cellular Stress ◽

Cellular Stress Response ◽

C Elegans ◽

Arsenic Copper ◽

The Impact

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.

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C. elegans discriminate colors without eyes or opsins

10.1101/092072 ◽

2016 ◽

Cited By ~ 1

Author(s):

D. Dipon Ghosh ◽

Xin Jin ◽

Michael Nitabach

Keyword(s):

Detection System ◽

Color Discrimination ◽

Blue Pigment ◽

Light Sources ◽

Amber Light ◽

C Elegans ◽

Color Detection ◽

Psychophysical Studies ◽

Light Guides ◽

Foraging Decision

AbstractHere we establish that, contrary to expectations, Caenorhabditis elegans nematode worms possess a color discrimination system despite lacking any opsin or other known visible light photoreceptor genes. We found that white light guides C. elegans foraging decisions away from harmful bacteria that secrete a blue pigment toxin. Absorption of amber light by this blue pigment toxin alters the color of light sensed by the worm, and thereby triggers an increase in avoidance. By combining narrow-band blue and amber light sources, we demonstrated that detection of the specific blue:amber ratio by the worm guides its foraging decision. These behavioral and psychophysical studies thus establish the existence of a color detection system that is distinct from those of other animals.

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Faculty Opinions recommendation of Broad-spectrum anti-biofilm peptide that targets a cellular stress response.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.718410935.793495619 ◽

2014 ◽

Author(s):

Kim Lewis ◽

Brian Conlon

Keyword(s):

Stress Response ◽

Broad Spectrum ◽

Cellular Stress ◽

Cellular Stress Response

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Integration of temporal single cell cellular stress response activity with Logic-ODE modeling reveals activation of ATF4-CHOP axis as a critical predictor of drug-induced liver injury

Biochemical Pharmacology ◽

10.1016/j.bcp.2021.114591 ◽

2021 ◽

pp. 114591

Author(s):

Lukas Surya Wijaya ◽

Panuwat Trairatphisan ◽

Attila Gabor ◽

Marije Niemeijer ◽

Jason Keet ◽

...

Keyword(s):

Stress Response ◽

Liver Injury ◽

Single Cell ◽

Cellular Stress ◽

Cellular Stress Response ◽

Drug Induced ◽

Drug Induced Liver Injury

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Flavonoids: Potential Candidates for the Treatment of Neurodegenerative Disorders

Biomedicines ◽

10.3390/biomedicines9020099 ◽

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.

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Mitochondrien unter Stress: Die Rolle der Präsequenzprotease MPP

BIOspektrum ◽

10.1007/s12268-021-1589-1 ◽

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.

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

International Journal of Molecular Sciences ◽

10.3390/ijms22062941 ◽

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.

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Induction and transmission of oncogene-induced senescence

Cellular and Molecular Life Sciences ◽

10.1007/s00018-020-03638-0 ◽

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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