Phytoestrogens genistein and daidzein affect immunity in the nematode <i>Caenorhabditis elegans</i> via alterations of vitellogenin expression

Fischer, Meike; Regitz, Charlotte; Kahl, Mareike; Werthebach, Michael; Boll, Michael; Wenzel, U.

doi:10.1002/mnfr.201200006

Cited by 30 publications

(22 citation statements)

References 46 publications

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“…Nuclear hormone receptor family is a key to many important cellular processes, but the role of NHR family in DNA damageinduced programmed cell death remains elusive. Previous study showed that NHR-14/HNF4, which was thought to be an estrogenic hormone receptor [8], was involved in the immune response processes via regulation of vitellogenin expression [22]. In present report, we identified nhr-14/ HNF4 as an important member of NHR in regulation of DNA damage-induced apoptosis.…”

Section: Discussionsupporting

confidence: 49%

WITHDRAWN: Caenorhabditis elegans nuclear hormone receptor NHR-14, cooperates with p53/cep-1 to regulate DNA damage-induced apoptosis

Shen¹,

Kang²,

Zhuang³

et al. 2018

Oncotarget

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Nuclear hormone receptor is involved in transcription regulation and many important cellular processes including development and metabolism. However, the role of nuclear hormone receptor in DNA damage-induced apoptosis remains elusive. Here we reported that RNAi of nhr-14, which was thought to be an estrogenic hormone receptor in Caenorhabditis elegans, inhibited DNA damage-induced apoptosis in prmt-5(gk357), a C. elegans homolog of mammalian type II arginine methyltransferase PRMT5, after ionizing radiation. Deletion of nhr-14 led to decreased DNA damageinduced germline apoptosis, but not in the physiological programmed cell death. We also demonstrate that nhr-14 is not a checkpoint gene and functions downstream of the checkpoint pathway. Moreover, we show that nhr-14 regulates egl-1 and ced-13 transcription upon DNA damage. In addition, we provided evidence that NHR-14 forms a complex with CEP-1/p53 and may function as a cofactor of CEP-1/p53. These findings indicate that NHR-14 might cooperate with CEP-1/p53 to regulate DNA damage-induced apoptosis, which reveals a novel role for nuclear hormone receptor in apoptosis.

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Section: Discussionsupporting

confidence: 49%

WITHDRAWN: Caenorhabditis elegans nuclear hormone receptor NHR-14, cooperates with p53/cep-1 to regulate DNA damage-induced apoptosis

Shen¹,

Kang²,

Zhuang³

et al. 2018

Oncotarget

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“…C. elegans can be infected by many other bacterial strains (Couillault and Ewbank 2002; Sicard et al 2007; Engelmann et al 2011; Fischer et al 2012, 2013; Julien-Gau et al 2014). Here we showed that P. luminescens TT01 was also highly pathogenic to C. elegans .…”

Section: Resultsmentioning

confidence: 99%

“…Although several studies have indicated that some P. luminescens strains displayed pathogenicity toward C. elegans (Couillault and Ewbank 2002; Sicard et al 2007; Engelmann et al 2011; Fischer et al 2012, 2013; Julien-Gau et al 2014), detailed phenotypes and the roles of host defenses have not been characterized. In this study we tested the pathogenicity of P. luminescens TT01, a mutualistic bacterial strain of the H. bacteriophora TT01 to C. elegans .…”

Section: Introductionmentioning

confidence: 99%

Activated and inactivated immune responses in Caenorhabditis elegans against Photorhabdus luminescens TT01

2014

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The Gram-negative bacterium Photorhabdus luminescens which symbiotically associates with the entomopathogenic nematode Heterorhabditis bacteriophora, has a broad insecticidal and nematicidal activity. The virulence of P. luminescens toward the non-mutualistic nematode Caenorhabditis elegans has not been described. We showed that when fed on P. luminescens, the intestinal cells of C. elegans worms become delicate and some crystal-like structure was developed within the intestinal lumen. Next, we examined the requirement of the p38 mitogen-activated protein kinase (MAPK) and insulin/IGF-1 signaling pathway against P. luminescens. Depletion of pmk-1 by RNAi enhances susceptibility to P. luminescens, and numerous downstream targets regulated by the p38 MAPK pathway were induced when fed on P. luminescens. On the other hand, knockdown of daf-16 has no effects on C. elegans lifespan, but knockdown of daf-2 dramatically increased resistance to P. luminescens in a daf-16-dependent manner. We also revealed one of the daf-2 ligands ins-7 was induced and ins-7 deletion mutant survived longer when fed on P. luminescens. These results suggest the p38 MAPK pathway is activated and required for the host defense against P. luminescens. Insulin/IGF-1 signaling pathway is inactivated by P. luminescens through the overexpression of insulin-like gene.Electronic supplementary materialThe online version of this article (doi:10.1186/2193-1801-3-274) contains supplementary material, which is available to authorized users.

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“…Lipid metabolism is an important pathway associated with aging (Nakamura et al, 1999; Gubert et al, 2016). Besides providing energy for developing embryos, VITs are involved in the stress response in diverse organisms (Fischer et al, 2012). VITs were found to act as acute- phase-proteins and to possess bacterial binding and inhibiting activities in different fish-species (Zhang, 2011; Fischer et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

The Shift of the Intestinal Microbiome in the Innate Immunity-Deficient Mutant rde-1 Strain of C. elegans upon Orsay Virus Infection

et al. 2017

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The status of intestinal microbiota is a determinant of host health. However, the alteration of the gut microbiota caused by the innate immune response to virus infection is unclear. Caenorhabditis elegans and its natural virus Orsay provide an excellent model of host–virus interactions. We evaluated the intestinal microbial community complexity of the wild-type N2 and the innate immunity-deficient mutant rde-1 (ne219) strains of C. elegans upon Orsay virus infection. The gut microbiota diversity was decreased in rde-1 (ne219) mutant animals, and a large number of genes were associated with the difference between infected and uninfected rde-1 (ne219) mutant animals. Therefore, this study provides the first evaluation of the alterations caused by Orsay virus on intestinal microbiota in wildtype and innate immunity-deficient animals using C. elegans as the model species. Our findings indicate that virus infection may alters the microbiome in animals with defective immune response.

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Phytoestrogens genistein and daidzein affect immunity in the nematode Caenorhabditis elegans via alterations of vitellogenin expression

Abstract: Our studies show that induction of estrogen-responsive vitellogenin(s) by the phytoestrogen daidzein potently increases resistance of C. elegans versus pathogenic bacteria and heat whereas genistein acts in an antiestrogenic manner.

Cited by 30 publications

References 46 publications

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

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

Activated and inactivated immune responses in Caenorhabditis elegans against Photorhabdus luminescens TT01

The Shift of the Intestinal Microbiome in the Innate Immunity-Deficient Mutant rde-1 Strain of C. elegans upon Orsay Virus Infection

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