PKG and NHR-49 signalling co-ordinately regulate short-term fasting-induced lysosomal lipid accumulation in C. elegans

2014 ◽  
Vol 461 (3) ◽  
pp. 509-520 ◽  
Author(s):  
Wen-ming Huang ◽  
Zhao-yu Li ◽  
Yan-jun Xu ◽  
Wei Wang ◽  
Mao-ge Zhou ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Lipid Accumulation ◽  
Hormone Receptor ◽  
Nuclear Hormone Receptor ◽  
Protein Kinase G ◽  
Short Term ◽  
C Elegans ◽  
Lipids Accumulation

Short-term fasting induces lipids accumulation in the lysosome of C. elegans and the response is co-ordinately regulated by protein kinase G and nuclear hormone receptor NHR-49-mediated pathways.

scholarly journals Nuclear Hormone Receptor Regulation of MicroRNAs Controls Innate Immune Responses in C. elegans

2013 ◽  
Vol 9 (8) ◽  
pp. e1003545 ◽  
Author(s):  
Feng Liu ◽  
Chen-Xi He ◽  
Li-Jun Luo ◽  
Quan-Li Zou ◽  
Yong-Xu Zhao ◽  
...  
Keyword(s):  
Immune Responses ◽  
Hormone Receptor ◽  
Nuclear Hormone Receptor ◽  
Innate Immune ◽  
Receptor Regulation ◽  
Innate Immune Responses ◽  
C Elegans

scholarly journals Nuclear Hormone Receptor NHR-49 Controls Fat Consumption and Fatty Acid Composition in C. elegans

PLoS Biology ◽  
2005 ◽  
Vol 3 (2) ◽  
pp. e53 ◽  
Author(s):  
Marc R. Van Gilst ◽  
Haralambos Hadjivassiliou ◽  
Amber Jolly ◽  
Keith R Yamamoto
Keyword(s):  
Fatty Acid Composition ◽  
Fatty Acid ◽  
Acid Composition ◽  
Hormone Receptor ◽  
Nuclear Hormone Receptor ◽  
C Elegans ◽  
Fat Consumption

scholarly journals Nuclear hormone receptor DHR96 mediates the resistance to xenobiotics but not the increased lifespan of insulin-mutant Drosophila

2016 ◽  
Vol 113 (5) ◽  
pp. 1321-1326 ◽  
Author(s):  
Sonita Afschar ◽  
Janne M. Toivonen ◽  
Julia Marianne Hoffmann ◽  
Luke Stephen Tain ◽  
Daniela Wieser ◽  
...  
Keyword(s):  
Hormone Receptor ◽  
Fruit Fly ◽  
Xenobiotic Metabolism ◽  
Nuclear Hormone Receptor ◽  
Laboratory Animals ◽  
Dietary Interventions ◽  
Gene Encoding ◽  
Transgenic Expression ◽  
C Elegans ◽  
Lipophilic Toxins

Lifespan of laboratory animals can be increased by genetic, pharmacological, and dietary interventions. Increased expression of genes involved in xenobiotic metabolism, together with resistance to xenobiotics, are frequent correlates of lifespan extension in the nematode worm Caenorhabditis elegans, the fruit fly Drosophila, and mice. The Green Theory of Aging suggests that this association is causal, with the ability of cells to rid themselves of lipophilic toxins limiting normal lifespan. To test this idea, we experimentally increased resistance of Drosophila to the xenobiotic dichlordiphenyltrichlorethan (DDT), by artificial selection or by transgenic expression of a gene encoding a cytochrome P450. Although both interventions increased DDT resistance, neither increased lifespan. Furthermore, dietary restriction increased lifespan without increasing xenobiotic resistance, confirming that the two traits can be uncoupled. Reduced activity of the insulin/Igf signaling (IIS) pathway increases resistance to xenobiotics and extends lifespan in Drosophila, and can also increase longevity in C. elegans, mice, and possibly humans. We identified a nuclear hormone receptor, DHR96, as an essential mediator of the increased xenobiotic resistance of IIS mutant flies. However, the IIS mutants remained long-lived in the absence of DHR96 and the xenobiotic resistance that it conferred. Thus, in Drosophila IIS mutants, increased xenobiotic resistance and enhanced longevity are not causally connected. The frequent co-occurrence of the two traits may instead have evolved because, in nature, lowered IIS can signal the presence of pathogens. It will be important to determine whether enhanced xenobiotic metabolism is also a correlated, rather than a causal, trait in long-lived mice.

scholarly journals The nuclear hormone receptor NHR-86 controls anti-pathogen responses in C. elegans

PLoS Genetics ◽  
2019 ◽  
Vol 15 (1) ◽  
pp. e1007935 ◽  
Author(s):  
Nicholas D. Peterson ◽  
Hilary K. Cheesman ◽  
Pengpeng Liu ◽  
Sarah M. Anderson ◽  
Kyle J. Foster ◽  
...  
Keyword(s):  
Hormone Receptor ◽  
Nuclear Hormone Receptor ◽  
C Elegans

scholarly journals The C. elegans miR-235 regulates the toxicity of graphene oxide via targeting the nuclear hormone receptor DAF-12 in the intestine

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Tiantian Guo ◽  
Lu Cheng ◽  
Huimin Zhao ◽  
Yingying Liu ◽  
Yunhan Yang ◽  
...  
Keyword(s):  
Graphene Oxide ◽  
Signaling Pathway ◽  
Hormone Receptor ◽  
Molecular Basis ◽  
Mapk Signaling ◽  
Nuclear Hormone Receptor ◽  
In Vivo Model ◽  
Protective Mechanism ◽  
C Elegans

Abstract The increased application of graphene oxide (GO), a new carbon-based engineered nanomaterial, has generated a potential toxicity in humans and the environment. Previous studies have identified some dysregulated microRNAs (miRNAs), such as up-regulated mir-235, in organisms exposed to GO. However, the detailed mechanisms of the dysregulation of miRNA underlying GO toxicity are still largely elusive. In this study, we employed Caenorhabditis elegans as an in vivo model to investigate the biological function and molecular basis of mir-235 in the regulation of GO toxicity. After low concentration GO exposure, mir-235 (n4504) mutant nematodes were sensitive to GO toxicity, implying that mir-235 mediates a protection mechanism against GO toxicity. Tissue-specific assays suggested that mir-235 expressed in intestine is required for suppressing the GO toxicity in C. elegans. daf-12, a gene encoding a member of the steroid hormone receptor superfamily, acts as a target gene of mir-235 in the nematode intestine in response to GO treatment, and RNAi knockdown of daf-12 suppressed the sensitivity of mir-235(n4503) to GO toxicity. Further genetic analysis showed that DAF-12 acted in the upstream of DAF-16 in insulin/IGF-1 signaling pathway and PMK-1 in p38 MAPK signaling pathway in parallel to regulate GO toxicity. Altogether, our results revealed that mir-235 may activate a protective mechanism against GO toxicity by suppressing the DAF-12-DAF-16 and DAF-12-PMK-1 signaling cascade in nematodes, which provides an important molecular basis for the in vivo toxicity of GO at the miRNA level.

scholarly journals Regulation of C. elegans Fat Uptake and Storage by Acyl-CoA Synthase-3 Is Dependent on NR5A Family Nuclear Hormone Receptor nhr-25

2010 ◽  
Vol 12 (4) ◽  
pp. 398-410 ◽  
Author(s):  
Brendan C. Mullaney ◽  
Raymond D. Blind ◽  
George A. Lemieux ◽  
Carissa L. Perez ◽  
Ida C. Elle ◽  
...  
Keyword(s):  
Hormone Receptor ◽  
Nuclear Hormone Receptor ◽  
C Elegans ◽  
Fat Uptake ◽  
And Storage

scholarly journals Comparative Metabolomics Reveals Endogenous Ligands of DAF-12, a Nuclear Hormone Receptor, Regulating C. elegans Development and Lifespan

2014 ◽  
Vol 19 (1) ◽  
pp. 73-83 ◽  
Author(s):  
Parag Mahanti ◽  
Neelanjan Bose ◽  
Axel Bethke ◽  
Joshua C. Judkins ◽  
Joshua Wollam ◽  
...  
Keyword(s):  
Hormone Receptor ◽  
Nuclear Hormone Receptor ◽  
Endogenous Ligands ◽  
C Elegans ◽  
Comparative Metabolomics

scholarly journals Opposing steroid signals modulate protein homeostasis through deep changes in fat metabolism in Caenorhabditis elegans

2019 ◽  
Author(s):  
Ana Pilar Gomez Escribano ◽  
Carlos Mora-Martinez ◽  
Marta Roca ◽  
Denise Walker ◽  
Joaquin Panadero ◽  
...  
Keyword(s):  
Huntington Disease ◽  
Hormone Receptor ◽  
Fat Metabolism ◽  
Nuclear Hormone Receptor ◽  
Protein Homeostasis ◽  
Spinocerebellar Ataxias ◽  
C Elegans ◽  
Expression Of Genes ◽  
Β Amyloid ◽  
Polyq Diseases

Protein homeostasis is crucial for viability of all organisms, and mutations that enhance protein aggregation cause different human pathologies, including polyglutamine (polyQ) diseases, such as some spinocerebellar ataxias or Huntington disease. Here, we report that neuronal Stomatin-like protein UNC-1 protects against aggregation of prone-to-aggregate proteins, like polyQs, α-synuclein and β-amyloid, in C. elegans. UNC-1, in IL2 neurons, antagonizes the function of the cytosolic sulfotransferase SSU-1 in neurohormonal signalling from ASJ neurons. The target of this hormone is the nuclear hormone receptor NHR-1, which acts cell-autonomously to protect from aggregation in muscles. A second nuclear hormone receptor, DAF-12, functions oppositely to NHR-1 to maintain protein homeostasis. Transcriptomics analyses reveal deep changes in the expression of genes involved in fat metabolism, in unc-1 mutants, which are regulated by NHR-1. This suggest that fat metabolism changes, controlled by neurohormonal signalling, contributes to modulate protein homeostasis.

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