scholarly journals Retraction Notice to: Gut-Colonizing Bacteria Promote C. elegans Innate Immunity by Producing Nitric Oxide

Cell Reports ◽  
2016 ◽  
Vol 15 (5) ◽  
pp. 1123 ◽  
Author(s):  
Yi Xiao ◽  
Fang Liu ◽  
Zhigang Zhang ◽  
Jie Tang ◽  
Cheng-Gang Zou ◽  
...  
Cell Reports ◽  
2016 ◽  
Vol 14 (6) ◽  
pp. 1301-1307 ◽  
Author(s):  
Yi Xiao ◽  
Fang Liu ◽  
Zhigang Zhang ◽  
Jie Tang ◽  
Cheng-Gang Zou ◽  
...  

2008 ◽  
Vol 148 (2) ◽  
pp. 818-828 ◽  
Author(s):  
Wei Ma ◽  
Andries Smigel ◽  
Yu-Chang Tsai ◽  
Janet Braam ◽  
Gerald A. Berkowitz
Keyword(s):  

2021 ◽  
Author(s):  
Hua Bai ◽  
Wei Zou ◽  
Wenhui Zhou ◽  
Keqin Zhang ◽  
Xiaowei Huang

To antagonize infection of pathogenic bacteria in soil and confer increased survival, Caenorhabditis elegans employs innate immunity and behavioral avoidance synchronously as the two main defensive strategies. Although both biological processes and their individual signaling pathways have been partially elucidated, knowledge of their interrelationship remains limited. The current study reveals that deficiency of innate immunity triggered by mutation of the classic immune gene pmk-1 promotes avoidance behavior in C. elegans ; and vice versa. Restoration of pmk-1 expression using the tissue-specific promoters suggested that the functional loss of both intestinal and neuronal pmk-1 is necessary for the enhanced avoidance. Additionally, PMK-1 co-localized with the E3 ubiquitin ligase HECW-1 in OLL neurons and regulated the expressional level of the latter, which consequently affected the production of NPR-1, a G-protein-coupled receptor homologous to the mammalian neuropeptide Y receptor, in RMG neurons in a non-cell-autonomous manner. Collectively, our study illustrates, once the innate immunity is impaired when C. elegans antagonizes bacterial infection, the other defensive strategy of behavioral avoidance can be enhanced accordingly via the HECW-1/NPR-1 module, suggesting that GPCRs in neural circuits may receive the inputs from immune system and integrate those two systems for better adapting to the real-time status.


2021 ◽  
Author(s):  
Bhoomi Madhu ◽  
Tina L. Gumienny

Innate immunity in animals is orchestrated by multiple cell signaling pathways, including the TGF-β; superfamily pathway. While the role of TGF-β signaling in innate immunity has been clearly identified, the requirement for this pathway in generating specific, robust responses to different bacterial challenges has not been characterized. Here, we address the role of DBL-1/TGF-β in regulating signature host defense responses to a wide range of bacteria in C. elegans. This work reveals a role of DBL-1/TGF-β in animal survival, organismal behaviors, and molecular responses in different environments. Additionally, we identify a novel role for SMA-4/Smad that suggests both DBL-1/TGF-β-dependent and -independent functions in host avoidance responses. RNA-seq analyses and immunity reporter studies indicate DBL-1/TGF-β differentially regulates target gene expression upon exposure to different bacteria. Furthermore, the DBL-1/TGF-β pathway is itself differentially affected by the bacteria exposure. Collectively, these findings demonstrate bacteria-specific host immune responses regulated by the DBL-1/TGF-β signaling pathway.


2021 ◽  
Author(s):  
Phillip Wibisono ◽  
Shawndra Wibisono ◽  
Jan Watteyne ◽  
Chia-Hui Chen ◽  
Durai Sellegounder ◽  
...  

A key question in current immunology is how the innate immune system generates high levels of specificity. Like most invertebrates, Caenorhabditis elegans does not have an adaptive immune system and relies solely on innate immunity to defend itself against pathogen attacks, yet it can still differentiate different pathogens and launch distinct innate immune responses. Here, we have found that functional loss of NMUR-1, a neuronal GPCR homologous to mammalian receptors for the neuropeptide neuromedin U, has diverse effects on C. elegans survival against various bacterial pathogens. Transcriptomic analyses and functional assays revealed that NMUR-1 modulates C. elegans transcription activity by regulating the expression of transcription factors, which, in turn, controls the expression of distinct immune genes in response to different pathogens. Our study has uncovered a molecular basis for the specificity of C. elegans innate immunity that could provide mechanistic insights into understanding the specificity of vertebrate innate immunity.


2021 ◽  
Vol 35 (S1) ◽  
Author(s):  
Annabel Lee ◽  
Antonio Rua ◽  
Shallee Page

2009 ◽  
Vol 5 (5) ◽  
pp. 450-462 ◽  
Author(s):  
Akwasi Anyanful ◽  
Kirk A. Easley ◽  
Guy M. Benian ◽  
Daniel Kalman

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