scholarly journals IGLR-2, a Leucine-Rich Repeat Domain Containing Protein, Is Required for the Host Defense in Caenorhabditis elegans

2020 ◽  
Vol 11 ◽  
Author(s):  
Cheng-Ju Kuo ◽  
Ya-Chu Hsu ◽  
Sin-Tian Wang ◽  
Bang-Yu Liou ◽  
Serene Boon-Yuean Lim ◽  
...  

Enterohemorrhagic Escherichia coli (EHEC), a human pathogen, also infects Caenorhabditis elegans. We demonstrated previously that C. elegans activates the p38 MAPK innate immune pathway to defend against EHEC infection. However, whether a C. elegans pattern recognition receptor (PRR) exists to regulate the immune pathway remains unknown. PRRs identified in other metazoans contain several conserved domains, including the leucine-rich repeat (LRR). By screening a focused RNAi library, we identified the IGLR-2, a transmembrane protein containing the LRR domain, as a potential immune regulator in C. elegans. Our data showed that iglr-2 regulates the host susceptibility to EHEC infection. Moreover, iglr-2 is required for pathogen avoidance to EHEC. The iglr-2 overexpressed strain, which was more resistant to EHEC originally, showed hypersusceptibility to EHEC upon knockdown of the p38 MAPK pathway. Together, our data suggested that iglr-2 plays an important role in C. elegans to defend EHEC by regulating pathogen-avoidance behavior and the p38 MAPK pathway.

2020 ◽  
Vol 22 (10) ◽  
Author(s):  
Xiaowen Huang ◽  
Wen Pan ◽  
Wooseong Kim ◽  
Alexis White ◽  
Silei Li ◽  
...  

PLoS ONE ◽  
2014 ◽  
Vol 9 (7) ◽  
pp. e103290 ◽  
Author(s):  
Jessica Dinh ◽  
Joseph T. Angeloni ◽  
Daniel B. Pederson ◽  
Xiaoxia Wang ◽  
Min Cao ◽  
...  

2015 ◽  
Vol 112 (18) ◽  
pp. E2366-E2375 ◽  
Author(s):  
Zhiji Ren ◽  
Victor R. Ambros

Animals maintain their developmental robustness against natural stresses through numerous regulatory mechanisms, including the posttranscriptional regulation of gene expression by microRNAs (miRNAs). Caenorhabditis elegans miRNAs of the let-7 family (let-7-Fam) function semiredundantly to confer robust stage specificity of cell fates in the hypodermal seam cell lineages. Here, we show reciprocal regulatory interactions between let-7-Fam miRNAs and the innate immune response pathway in C. elegans. Upon infection of C. elegans larvae with the opportunistic human pathogen Pseudomonas aeruginosa, the developmental timing defects of certain let-7-Fam miRNA mutants are enhanced. This enhancement is mediated by the p38 MAPK innate immune pathway acting in opposition to let-7-Fam miRNA activity, possibly via the downstream Activating Transcription Factor-7 (ATF-7). Furthermore, let-7-Fam miRNAs appear to exert negative regulation on the worm’s resistance to P. aeruginosa infection. Our results show that the inhibition of pathogen resistance by let-7 involves downstream heterochronic genes and the p38 MAPK pathway. These findings suggest that let-7-Fam miRNAs are integrated into innate immunity gene regulatory networks, such that this family of miRNAs modulates immune responses while also ensuring robust timing of developmental events under pathogen stress.


2016 ◽  
Author(s):  
Jill M. Hoyt ◽  
Samuel K. Wilson ◽  
Madhuri Kasa ◽  
Jeremy S. Rise ◽  
Irini Topalidou ◽  
...  

AbstractGq is a heterotrimeric G protein that is widely expressed in neurons and regulates neuronal activity. To identify pathways regulating neuronal Gq signaling we performed a forward genetic screen in Caenorhabditis elegans for suppressors of activated Gq. One of the suppressors is an allele of sek-1, which encodes a mitogen-activated protein kinase kinase (MAPKK) in the p38 MAPK pathway. Here we show that sek-1 mutants have a slow locomotion rate and that sek-1 acts in acetylcholine neurons to modulate both locomotion rate and Gq signaling. Furthermore, we find that sek-1 acts in mature neurons to modulate locomotion. Using genetic and behavioral approaches we demonstrate that other components of the p38 MAPK pathway also play a positive role in modulating locomotion and Gq signaling. Finally, we find that mutants in the SEK-1 p38 MAPK pathway partially suppress an activated mutant of the sodium leak channel NCA-1/NALCN, a downstream target of Gq signaling. Our results suggest that the SEK-1 p38 pathway may modulate the output of Gq signaling through NCA-1.


2016 ◽  
Vol 7 (7) ◽  
pp. 3211-3223 ◽  
Author(s):  
Arumugam Kamaladevi ◽  
Krishnaswamy Balamurugan

In the present study, the effect of lactic acid bacteria was investigated at the molecular level using the model organismCaenorhabditis elegansagainstKlebsiella pneumoniae.


2008 ◽  
Vol 56 (1) ◽  
pp. 83-89 ◽  
Author(s):  
Ewa Jablonska ◽  
Wioletta Ratajczak ◽  
Jakub Jablonski

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