scholarly journals Ilex paraguariensis modulates fat metabolism in Caenorhabditis elegans through purinergic system (ADOR-1) and nuclear hormone receptor (NHR-49) pathways

PLoS ONE ◽  
2018 ◽  
Vol 13 (9) ◽  
pp. e0204023 ◽  
Author(s):  
Marina Lopes Machado ◽  
Leticia Priscilla Arantes ◽  
Priscila Gubert ◽  
Daniele Coradini Zamberlan ◽  
Thayanara Cruz da Silva ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Hormone Receptor ◽  
Fat Metabolism ◽  
Nuclear Hormone Receptor ◽  
Ilex Paraguariensis ◽  
Purinergic System

scholarly journals Repression of a Potassium Channel by Nuclear Hormone Receptor and TGF-β Signaling Modulates Insulin Signaling in Caenorhabditis elegans

PLoS Genetics ◽  
2012 ◽  
Vol 8 (2) ◽  
pp. e1002519 ◽  
Author(s):  
Donha Park ◽  
Karen L. Jones ◽  
Hyojin Lee ◽  
Terrance P. Snutch ◽  
Stefan Taubert ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Potassium Channel ◽  
Insulin Signaling ◽  
Hormone Receptor ◽  
Nuclear Hormone Receptor

scholarly journals Gain-of-Function Alleles in Caenorhabditis elegans Nuclear Hormone Receptor nhr-49 Are Functionally Distinct

PLoS ONE ◽  
2016 ◽  
Vol 11 (9) ◽  
pp. e0162708 ◽  
Author(s):  
Kayoung Lee ◽  
Grace Ying Shyen Goh ◽  
Marcus Andrew Wong ◽  
Tara Leah Klassen ◽  
Stefan Taubert
Keyword(s):  
Caenorhabditis Elegans ◽  
Hormone Receptor ◽  
Nuclear Hormone Receptor ◽  
Gain Of Function

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.

scholarly journals Caenorhabditis elegans methionine/S-adenosylmethionine cycle activity is sensed and adjusted by a nuclear hormone receptor

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Gabrielle E Giese ◽  
Melissa D Walker ◽  
Olga Ponomarova ◽  
Hefei Zhang ◽  
Xuhang Li ◽  
...  
Keyword(s):  
Gene Expression ◽  
Caenorhabditis Elegans ◽  
Vitamin B12 ◽  
Transcriptional Activation ◽  
Hormone Receptor ◽  
Metabolic Pathways ◽  
Nuclear Hormone Receptor ◽  
Dietary Vitamin ◽  
Independent Mechanism ◽  
Dependent Mechanism

Vitamin B12 is an essential micronutrient that functions in two metabolic pathways: the canonical propionate breakdown pathway and the methionine/S-adenosylmethionine (Met/SAM) cycle. In Caenorhabditis elegans, low vitamin B12, or genetic perturbation of the canonical propionate breakdown pathway results in propionate accumulation and the transcriptional activation of a propionate shunt pathway. This propionate-dependent mechanism requires nhr-10 and is referred to as ‘B12-mechanism-I’. Here, we report that vitamin B12 represses the expression of Met/SAM cycle genes by a propionate-independent mechanism we refer to as ‘B12-mechanism-II’. This mechanism is activated by perturbations in the Met/SAM cycle, genetically or due to low dietary vitamin B12. B12-mechanism-II requires nhr-114 to activate Met/SAM cycle gene expression, the vitamin B12 transporter, pmp-5, and adjust influx and efflux of the cycle by activating msra-1 and repressing cbs-1, respectively. Taken together, Met/SAM cycle activity is sensed and transcriptionally adjusted to be in a tight metabolic regime.

scholarly journals WITHDRAWN: Caenorhabditis elegans nuclear hormone receptor NHR-14, cooperates with p53/cep-1 to regulate DNA damage-induced apoptosis

Oncotarget ◽  
2018 ◽  
Vol 0 (0) ◽  
Author(s):  
Junling Shen ◽  
Jiaxin Kang ◽  
Zhuang Yao ◽  
Youli Jian ◽  
Yudong Jing ◽  
...  
Keyword(s):  
Dna Damage ◽  
Caenorhabditis Elegans ◽  
Hormone Receptor ◽  
Nuclear Hormone Receptor ◽  
Induced Apoptosis

CHR3: a Caenorhabditis elegans orphan nuclear hormone receptor required for proper epidermal development and molting

Development ◽  
1998 ◽  
Vol 125 (9) ◽  
pp. 1617-1626 ◽  
Author(s):  
M. Kostrouchova ◽  
M. Krause ◽  
Z. Kostrouch ◽  
J.E. Rall
Keyword(s):  
Caenorhabditis Elegans ◽  
Hormone Receptor ◽  
Nuclear Protein ◽  
Cell Function ◽  
Reporter Genes ◽  
Postembryonic Development ◽  
Nuclear Hormone Receptor ◽  
Hormone Response ◽  
Gene Encoding ◽  
Inducible Gene

CHR3 is a Caenorhabditis elegans orphan nuclear hormone receptor highly homologous to Drosophila DHR3, an ecdysone-inducible gene product involved in metamorphosis. Related vertebrate factors include RORalpha/RZRalpha, RZRbeta and RevErb. Gel-shift studies show that CHR3 can bind the DR5-type hormone response sequence. CHR3 is a nuclear protein present in all blastomeres during early embryogenesis. During morphogenesis, both CHR3 protein and zygotically active reporter genes are detectable in epidermal cells and their precursors. Inhibition of the gene encoding CHR3 results in several larval defects associated with abnormal epidermal cell function, including molting and body size regulation, suggesting that CHR3 is an essential epidermal factor required for proper postembryonic development.

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