scholarly journals piRNA-associated proteins and retrotransposons are differentially expressed in murine testis and ovary of aryl hydrocarbon receptor deficient mice

Open Biology ◽  
2016 ◽  
Vol 6 (12) ◽  
pp. 160186 ◽  
Author(s):  
Eva M. Rico-Leo ◽  
Nuria Moreno-Marín ◽  
Francisco J. González-Rico ◽  
Eva Barrasa ◽  
Cristina Ortega-Ferrusola ◽  
...  
Keyword(s):  
Transposable Elements ◽  
Germ Cell ◽  
Aryl Hydrocarbon Receptor ◽  
Cell Maturation ◽  
Ovary Development ◽  
Aryl Hydrocarbon ◽  
Sperm Counts ◽  
Associated Proteins ◽  
Pachytene Spermatocytes ◽  
Deficient Mice

Previous studies suggested that the aryl hydrocarbon receptor (AhR) contributes to mice reproduction and fertility. However, the mechanisms involved remain mostly unknown. Retrotransposon silencing by Piwi-interacting RNAs (piRNAs) is essential for germ cell maturation and, remarkably, AhR has been identified as a regulator of murine B1-SINE retrotransposons. Here, using littermate AhR +/+ and AhR −/− mice, we report that AhR regulates the general course of spermatogenesis and oogenesis by a mechanism likely to be associated with piRNA-associated proteins, piRNAs and retrotransposons. piRNA-associated proteins MVH and Miwi are upregulated in leptotene to pachytene spermatocytes with a more precocious timing in AhR −/− than in AhR +/+ testes. piRNAs and transcripts from B1-SINE , LINE-1 and IAP retrotransposons increased at these meiotic stages in AhR-null testes. Moreover, B1-SINE transcripts colocalize with MVH and Miwi in leptonema and pachynema spermatocytes. Unexpectedly, AhR −/− males have increased sperm counts, higher sperm functionality and enhanced fertility than AhR +/+ mice. In contrast, piRNA-associated proteins and B1-SINE and IAP -derived transcripts are reduced in adult AhR −/− ovaries. Accordingly, AhR-null female mice have lower numbers of follicles when compared with AhR +/+ mice. Thus, AhR deficiency differentially affects testis and ovary development possibly by a process involving piRNA-associated proteins, piRNAs and transposable elements.

Aryl-hydrocarbon Receptor-Deficient Mice Are Resistant to 2,3,7,8-Tetrachlorodibenzo-p-dioxin-Induced Toxicity

1996 ◽  
Vol 140 (1) ◽  
pp. 173-179 ◽  
Author(s):  
Pedro M. Fernandez-Salguero ◽  
David M. Hilbert ◽  
Stuart Rudikoff ◽  
Jerrold M. Ward ◽  
Frank J. Gonzalez
Keyword(s):  
Aryl Hydrocarbon Receptor ◽  
Aryl Hydrocarbon ◽  
Tetrachlorodibenzo P Dioxin ◽  
Deficient Mice

scholarly journals Acyloxyacyl hydrolase modulates depressive-like behaviors through aryl hydrocarbon receptor

2019 ◽  
Vol 317 (2) ◽  
pp. R289-R300 ◽  
Author(s):  
Lizath M. Aguiniga ◽  
Wenbin Yang ◽  
Ryan E. Yaggie ◽  
Anthony J. Schaeffer ◽  
David J. Klumpp ◽  
...  
Keyword(s):  
Aryl Hydrocarbon Receptor ◽  
Therapeutic Target ◽  
Binding Sites ◽  
Hypothalamic Pituitary Adrenal ◽  
Adrenal Axis ◽  
Aryl Hydrocarbon ◽  
Acyloxyacyl Hydrolase ◽  
Deficient Mice ◽  
Pituitary Adrenal Axis

Corticotropin-releasing factor (CRF) regulates stress responses, and aberrant CRF signals are associated with depressive disorders. Crf expression is responsive to arachidonic acid (AA), where CRF is released from the hypothalamic paraventricular nucleus (PVN) to initiate the hypothalamic-pituitary-adrenal axis, culminating in glucocorticoid stress hormone release. Despite this biological and clinical significance, Crf regulation is unclear. Here, we report that acyloxyacyl hydrolase, encoded by Aoah, is expressed in the PVN, and Aoah regulates Crf through the aryl hydrocarbon receptor (AhR). We previously showed that AOAH-deficient mice mimicked interstitial cystitis/bladder pain syndrome, a condition frequently associated with comorbid anxiety and depression. With the use of novelty-suppressed feeding and sucrose preference assays to quantify rodent correlates of anxiety/depression, AOAH-deficient mice exhibited depressive behaviors. AOAH-deficient mice also had increased CNS AA, increased Crf expression in the PVN, and elevated serum corticosterone, consistent with dysfunction of the hypothalamic-pituitary-adrenal axis. The human Crf promoter has putative binding sites for AhR and peroxisome proliferator-activated receptor (PPARγ). PPARγ did not affect AA-dependent Crf expression in vitro, and conditional Pparγ knockout did not alter the AOAH-deficient depressive phenotype, despite previous studies implicating PPARγ as a therapeutic target for depression. In contrast, Crf induction was mediated by AhR binding sites in vitro and increased by AhR overexpression. Furthermore, conditional Ahr knockout rescued the depressive phenotype of AOAH-deficient mice. Finally, an AhR antagonist rescued the AOAH-deficient depressive phenotype. Together, our results demonstrate that Aoah is a novel genetic regulator of Crf mediated through AhR, and AhR is a therapeutic target for depression.

Aryl hydrocarbon receptor-deficient mice are protected from high fat diet-induced changes in metabolic rhythms

2017 ◽  
Vol 34 (3) ◽  
pp. 318-336 ◽  
Author(s):  
Cassie Jaeger ◽  
Canxin Xu ◽  
Mingwei Sun ◽  
Stacey Krager ◽  
Shelley A. Tischkau
Keyword(s):  
Aryl Hydrocarbon Receptor ◽  
High Fat Diet ◽  
High Fat ◽  
Aryl Hydrocarbon ◽  
Induced Changes ◽  
Deficient Mice

scholarly journals The Group 3 Innate Lymphoid Cell Defect in Aryl Hydrocarbon Receptor Deficient Mice Is Associated with T Cell Hyperactivation during Intestinal Infection

PLoS ONE ◽  
2015 ◽  
Vol 10 (5) ◽  
pp. e0128335 ◽  
Author(s):  
Sagie Wagage ◽  
Gretchen Harms Pritchard ◽  
Lucas Dawson ◽  
Elizabeth L. Buza ◽  
Gregory F. Sonnenberg ◽  
...  
Keyword(s):  
T Cell ◽  
Aryl Hydrocarbon Receptor ◽  
Lymphoid Cell ◽  
Intestinal Infection ◽  
Innate Lymphoid Cell ◽  
Aryl Hydrocarbon ◽  
Group 3 ◽  
Deficient Mice ◽  
Cell Defect

scholarly journals Association between polymorphisms in the aryl hydrocarbon receptor repressor gene and disseminated testicular germ cell cancer

2013 ◽  
Vol 4 ◽  
Author(s):  
Leon J. S. Brokken ◽  
Yvonne Lundberg-Giwercman ◽  
Ewa Rajpert-De Meyts ◽  
Jakob Eberhard ◽  
Olof Ståhl ◽  
...  
Keyword(s):  
Germ Cell ◽  
Aryl Hydrocarbon Receptor ◽  
Cell Cancer ◽  
Germ Cell Cancer ◽  
Testicular Germ Cell ◽  
Repressor Gene ◽  
Aryl Hydrocarbon ◽  
Testicular Germ Cell Cancer

scholarly journals A42 MICROBIAL METABOLISM OF DIETARY TRYPTOPHAN ENHANCES ARYL HYDROCARBON RECEPTOR ACTIVATION: IMPLICATIONS FOR IBD

2020 ◽  
Vol 3 (Supplement_1) ◽  
pp. 50-51
Author(s):  
L Rondeau ◽  
A V Clarizio ◽  
J Jury ◽  
D L Gibson ◽  
P Bercik ◽  
...  
Keyword(s):  
16S Rrna ◽  
Gut Microbiota ◽  
Aryl Hydrocarbon Receptor ◽  
Healthy Subjects ◽  
Tryptophan Metabolism ◽  
Luciferase Reporter ◽  
Reporter Assay ◽  
Aryl Hydrocarbon ◽  
Deficient Mice ◽  
Activation Capacity

Abstract Background Intestinal immune homeostasis is maintained by the interplay between microbiota and the mucosal immune system. Changes in gut microbiota have been associated with chronic intestinal conditions, such as inflammatory bowel disease (IBD). The aryl hydrocarbon receptor (AhR) is a transcription factor that is activated by dietary and environmental stimuli to control immune responses in the gut and homeostatic mechanisms at mucosal surfaces. In IBD, AhR expression is downregulated. Major agonists of AhR in the gut include microbial tryptophan metabolites such as indole derivatives, which are decreased in IBD patients. The mechanisms involved in tryptophan metabolism by bacteria and their implications in AhR activation and thus IBD pathogenesis are not well understood. Aims To investigate whether tryptophan metabolism by intestinal bacteria participates in AhR activation and IBD pathogenesis. Methods Microbiota profiles (16S rRNA Illumina) and activation of AhR (luciferase reporter assay) were determined in fecal samples from IBD patients (n=10) and healthy volunteers (n=10). Germ-free C57BL/6 mice were colonized with fecal slurries of 2 healthy subjects and 4 IBD patients (n=4 mice/donor) by oral gavage (humanized-mice). All mice were fed irradiated tryptophan diets with 0.1% or 1% tryptophan content for 14 days. Simultaneously, SPF Mucin 2 (Muc2) deficient mice (C57BL/6 background), which develop colitis spontaneously, were fed tryptophan diets (0.1%, 0.3% and 1% content). Activation of AhR was measured in feces using an AhR luciferase reporter assay. Inflammation was determined by immunohistochemistry and the characterization of immune infiltrate in colon cross-sections. Bacteria from human and mouse fecal samples were isolated and screened for their ability to produce indoles using biochemical reagents. Positive bacteria were identified by colony PCR and 16S rRNA Sanger sequencing. Results IBD patients had an altered fecal microbiota with a lower capacity to activate AhR compared to healthy subjects. Colonization of mice with microbiota from healthy subjects induced greater activation of AhR compared to mice colonized with microbiota from patients with IBD. Furthermore, increasing dietary tryptophan composition rescued the capacity to activate AhR. In Muc2 deficient mice, dietary tryptophan treatment enhanced AhR activation capacity and reduced infiltration of innate immune cells before the onset of colitis. Several AhR agonist producing bacterial species were identified and will be used in future experiments. Conclusions Activation of AhR is dependent on the gut microbiota and disease status of the donor. Dietary intervention with tryptophan enhances AhR activation capacity and may be a potential therapeutic avenue in IBD individuals with intestinal dysbiosis. Funding Agencies Farncombe Family Digestive Health Research Institute, Biocodex Microbiota Foundation

scholarly journals Activation of the aryl hydrocarbon receptor by a component of cigarette smoke reduces germ cell proliferation in the human fetal ovary

2015 ◽  
Vol 21 (9) ◽  
pp. 753-753 ◽  
Author(s):  
Richard A. Anderson ◽  
Luke McIlwain ◽  
Shiona Coutts ◽  
Hazel L. Kinnell ◽  
Paul A. Fowler ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Germ Cell ◽  
Aryl Hydrocarbon Receptor ◽  
Cigarette Smoke ◽  
Aryl Hydrocarbon ◽  
Fetal Ovary ◽  
Germ Cell Proliferation
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