scholarly journals Somatic aging pathways regulate reproductive plasticity in Caenorhabditis elegans

2019 ◽  
Author(s):  
Maria C. Ow ◽  
Alexandra M. Nichitean ◽  
Sarah E. Hall

SummaryEarly life stress of an animal often results in changes in gene expression that correspond with changes in their adult phenotype. In the nematode C. elegans, starvation during early larval stages promotes entry into a non-feeding, stress-resistant stage named dauer until environmental conditions improve. Here we show that the endocrine signaling attributed to the somatic aging pathways in C. elegans adults lacking a functional germline also regulate the reproductive phenotypes of adults that have experienced dauer as a result of early life starvation. Postdauer adults modulate their fatty acid metabolism in order to re-allocate fat reserves in a manner benefitting their progeny at the expense of the parental somatic fat reservoir. Our results also show that the metabolic plasticity in postdauer animals and the inheritance of ancestral starvation memory in the progeny are a result of crosstalk between somatic and reproductive tissues mediated by the HRDE-1 nuclear RNAi Argonaute.

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Maria C Ow ◽  
Alexandra M Nichitean ◽  
Sarah E Hall

In animals, early-life stress can result in programmed changes in gene expression that can affect their adult phenotype. In C. elegans nematodes, starvation during the first larval stage promotes entry into a stress-resistant dauer stage until environmental conditions improve. Adults that have experienced dauer (postdauers) retain a memory of early-life starvation that results in gene expression changes and reduced fecundity. Here we show that the endocrine pathways attributed to the regulation of somatic aging in C. elegans adults lacking a functional germline also regulate the reproductive phenotypes of postdauer adults that experienced early-life starvation. We demonstrate that postdauer adults reallocate fat to benefit progeny at the expense of the parental somatic fat reservoir and exhibit increased longevity compared to controls. Our results also show that the modification of somatic fat stores due to parental starvation memory is inherited in the F1 generation and may be the result of crosstalk between somatic and reproductive tissues mediated by the germline nuclear RNAi pathway.


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Eszter Gecse ◽  
Beatrix Gilányi ◽  
Márton Csaba ◽  
Gábor Hajdú ◽  
Csaba Sőti

AbstractStress exposure early in life is implicated in various behavioural and somatic diseases. Experiences during the critical perinatal period form permanent, imprinted memories promoting adult survival. Although imprinting is widely recognized to dictate behaviour, whether it actuates specific transcriptional responses at the cellular level is unknown. Here we report that in response to early life stresses, Caenorhabditis elegans nematodes form an imprinted cellular defense memory. We show that exposing newly-born worms to toxic antimycin A and paraquat, respectively, stimulates the expression of toxin-specific cytoprotective reporters. Toxin exposure also induces avoidance of the toxin-containing bacterial lawn. In contrast, adult worms do not exhibit aversive behaviour towards stress-associated bacterial sensory cues. However, the mere re-encounter with the same cues reactivates the previously induced cytoprotective reporters. Learned adult defenses require memory formation during the L1 larval stage and do not appear to confer increased protection against the toxin. Thus, exposure of C. elegans to toxic stresses in the critical period elicits adaptive behavioural and cytoprotective responses, which do not form imprinted aversive behaviour, but imprint a cytoprotective memory. Our findings identify a novel form of imprinting and suggest that imprinted molecular defenses might underlie various pathophysiological alterations related to early life stress.


2020 ◽  
Vol 21 (17) ◽  
pp. 6409
Author(s):  
Jichang Huang ◽  
Zhen Wu ◽  
Xumin Zhang

Exposure to mild early-life stresses can slow down aging, and protein phosphorylation might be an essential regulator in this process. However, the mechanisms of phosphorylation-based signaling networks during mild early-life stress remain elusive. Herein, we systematically analyzed the phosphoproteomes of Caenorhabditis elegans, which were treated with three mild temperatures (15 °C, 20 °C, and 25 °C) in two different short-term groups (10 min and 60 min). By utilizing an iTRAQ-based quantitative phosphoproteomic approach, 18,187 phosphosites from 3330 phosphoproteins were detected in this study. Volcano plots illustrated that the phosphorylation abundance of 374 proteins and 347 proteins, were significantly changed at 15 °C and 25 °C, respectively. Gene ontology, KEGG pathway and protein-protein interaction network analyses revealed that these phosphoproteins were primarily associated with metabolism, translation, development, and lifespan determination. A motif analysis of kinase substrates suggested that MAPK, CK, and CAMK were most likely involved in the adaption processes. Moreover, 16 and 14 aging-regulated proteins were found to undergo phosphorylation modifications under the mild stresses of 15 °C and 25 °C, respectively, indicating that these proteins might be important for maintaining long-term health. Further lifespan experiments confirmed that the candidate phosphoproteins, e.g., EGL-27 and XNP-1 modulated longevity at 15 °C, 20 °C, and 25 °C, and they showed increased tolerance to thermal and oxidative stresses. In conclusion, our findings offered data that supports understanding of the phosphorylation mechanisms involved in mild early-life stresses in C. elegans. Data are available via ProteomeXchange with identifier PXD021081.


2019 ◽  
Vol 133 (1) ◽  
pp. 50-58 ◽  
Author(s):  
Nathalie D. Elliott ◽  
Rick Richardson

2002 ◽  
Vol 7 (2) ◽  
pp. 89-95 ◽  
Author(s):  
David A Gutman ◽  
Charles B. Nemeroff

2019 ◽  
Vol 39 (5) ◽  
pp. 329-342
Author(s):  
Jamie Y. Choe ◽  
Maya Nair ◽  
Riyaz Basha ◽  
Byung-Jin Kim ◽  
Harlan P. Jones

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