Measurements of Physiological Stress Responses in &lt;em&gt;C. Elegans&lt;/em&gt;

Bar‐Ziv, Raz; Frakes, Ashley E.; Higuchi‐Sanabria, Ryo; Bolas, Theodore; Frankino, Phillip A.; Gildea, Holly K.; Metcalf, Melissa G.; Dillin, Andrew

doi:10.3791/61001

Cited by 30 publications

(38 citation statements)

References 60 publications

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“…Image acquisition was performed as previously described ( Bar-Ziv et al., 2020 ). Briefly, day 1 animals were picked under a standard dissection microscope onto a solid NGM plate that contained a ∼15μL drop of 100 nM sodium azide.…”

Section: Methodsmentioning

confidence: 99%

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SKN-1 regulates stress resistance downstream of amino catabolism pathways

et al. 2022

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Section: Methodsmentioning

confidence: 99%

“…To quantify fluorescence, a COPAS large particle biosorter was used as previously described ( Bar-Ziv et al., 2020 ). Data were collected gating for size (time of flight [TOF] and extinction) to exclude eggs and most L1 animals.…”

Section: Methodsmentioning

confidence: 99%

SKN-1 regulates stress resistance downstream of amino catabolism pathways

et al. 2022

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“…COPAS biosorting and analysis: Worm sorting using the COPAS biosorter (Union Biometrica) was performed as previously described (44). In brief, worms were heat shocked as described for hsp-16.2p::GFP conditions.…”

Section: Methodsmentioning

confidence: 99%

“…Synchronization: Worms were synchronized by bleaching as previously described (44). In brief, worms were collected off plates into 15mL conical tubes using M9 solution.…”

Section: Methodsmentioning

confidence: 99%

Glia of C. elegans coordinate the heat shock response independent of the neuronal thermosensory circuit and serotonin

Gildea

Frankino

Tronnes

et al. 2022

Preprint

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As organisms age, they lose the ability to induce appropriate stress responses, becoming vulnerable to protein toxicity and tissue damage. Neurons can signal to peripheral tissues to induce protective organelle-specific stress responses. Recent work has demonstrated a novel and independent role of glia in inducing such responses. Here, we show that overexpression of heat shock factor 1 (hsf-1) in the four astrocyte-like cephalic sheath cells of C. elegans is sufficient to induce a non-cell autonomous cytosolic unfolded protein response (UPR), also known as the heat shock response (HSR), in distal cells. These animals upregulate the HSR in peripheral cells and have increased lifespan and resistance to heat stress. This glial HSR regulation is independent of the canonical neuronal thermosensory circuit and of known neurotransmitters but is dependent on the small clear vesicle release protein UNC-13. Additionally, HSF-1 and the FOXO transcription factor DAF-16 are partially required in the peripheral tissues for increase of non-autonomous HSR, lifespan, and thermotolerance. We find that cephalic sheath glial hsf-1 over-expression leads to increased pathogen resistance, which suggests a role for this signaling pathway in immune function.

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“…The IRE-1 branch is primarily responsible for the induction of genes encoding ER resident chaperones, including hsp-4 and hsp-3 ( Shen et al, 2001 ). As such, the transcriptional reporter for hsp-4 has become one of the most common and robust methods of monitoring UPR ER activation within the nematode ( Calfon et al, 2002 ; Bar-Ziv et al, 2020b ). However, it is becoming increasingly clear that chaperone induction and protein homeostasis are not the only targets of UPR ER , as other critical processes are also induced including immune response, lysosomal function and autophagy, and lipid homeostasis.…”

Section: Introductionmentioning

confidence: 99%

Hijacking Cellular Stress Responses to Promote Lifespan

2022

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Organisms are constantly exposed to stress both from the external environment and internally within the cell. To maintain cellular homeostasis under different environmental and physiological conditions, cell have adapted various stress response signaling pathways, such as the heat shock response (HSR), unfolded protein responses of the mitochondria (UPRMT), and the unfolded protein response of the endoplasmic reticulum (UPRER). As cells grow older, all cellular stress responses have been shown to deteriorate, which is a major cause for the physiological consequences of aging and the development of numerous age-associated diseases. In contrast, elevated stress responses are often associated with lifespan extension and amelioration of degenerative diseases in different model organisms, including C. elegans. Activating cellular stress response pathways could be considered as an effective intervention to alleviate the burden of aging by restoring function of essential damage-clearing machinery, including the ubiquitin-proteosome system, chaperones, and autophagy. Here, we provide an overview of newly emerging concepts of these stress response pathways in healthy aging and longevity with a focus on the model organism, C. elegans.

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Measurements of Physiological Stress Responses in <em>C. Elegans</em>

Cited by 30 publications

References 60 publications

SKN-1 regulates stress resistance downstream of amino catabolism pathways

SKN-1 regulates stress resistance downstream of amino catabolism pathways

Glia of C. elegans coordinate the heat shock response independent of the neuronal thermosensory circuit and serotonin

Hijacking Cellular Stress Responses to Promote Lifespan

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