The C. elegans CCAAT-Enhancer-Binding Protein Gamma Is Required for Surveillance Immunity

Reddy, Kirthi C.; Dunbar, Tiffany L.; Nargund, Amrita M.; Haynes, Cole M.; Troemel, Emily R.

doi:10.1016/j.celrep.2016.01.055

Cited by 41 publications

(26 citation statements)

References 37 publications

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“…In particular, disruption of proteostasis often triggers this response in invertebrates 55 . For example, translation inhibition often occurs during microbial infection in worms 56 – 58 and flies 59 , resulting in immune activation. It is likely that mechanical damage, cellular disruption, or both is leading to immune activation in the epidermis and fat body here as well.…”

Section: Discussionmentioning

confidence: 99%

The heat shock response and humoral immune response are mutually antagonistic in honey bees

McKinstry

Chung

Truong

et al. 2017

Sci Rep

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The honey bee is of paramount importance to humans in both agricultural and ecological settings. Honey bee colonies have suffered from increased attrition in recent years, stemming from complex interacting stresses. Defining common cellular stress responses elicited by these stressors represents a key step in understanding potential synergies. The proteostasis network is a highly conserved network of cellular stress responses involved in maintaining the homeostasis of protein production and function. Here, we have characterized the Heat Shock Response (HSR), one branch of this network, and found that its core components are conserved. In addition, exposing bees to elevated temperatures normally encountered by honey bees during typical activities results in robust HSR induction with increased expression of specific heat shock proteins that was variable across tissues. Surprisingly, we found that heat shock represses multiple immune genes in the abdomen and additionally showed that wounding the cuticle of the abdomen results in decreased expression of multiple HSR genes in proximal and distal tissues. This mutually antagonistic relationship between the HSR and immune activation is unique among invertebrates studied to date and may promote understanding of potential synergistic effects of disparate stresses in this critical pollinator and social insects more broadly.

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Section: Discussionmentioning

confidence: 99%

The heat shock response and humoral immune response are mutually antagonistic in honey bees

McKinstry

Chung

Truong

et al. 2017

Sci Rep

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“…Interestingly, another C/EBP transcription factor, cebp-2 , has also recently been shown to play an important role in C. elegans translational defense. However, unlike CEBP-1, CEBP-2 promotes ToxA and P. aeruginosa protective mechanisms by acting as a heterodimeric transcription factor with ZIP-2 [34]. The ability of CEBP proteins to both promote and repress protective host defenses against the same pathogen demonstrates the range of CEBP immune functions and raises the question of whether, for example, CEBP-1 could be a positive effector under a different condition.…”

Section: Discussionmentioning

confidence: 99%

Tribbles ortholog NIPI-3 and bZIP transcription factor CEBP-1 regulate a Caenorhabditis elegans intestinal immune surveillance pathway

et al. 2016

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BackgroundMany pathogens secrete toxins that target key host processes resulting in the activation of immune pathways. The secreted Pseudomonas aeruginosa toxin Exotoxin A (ToxA) disrupts intestinal protein synthesis, which triggers the induction of a subset of P. aeruginosa-response genes in the nematode Caenorhabditis elegans.ResultsWe show here that one ToxA-induced C. elegans gene, the Tribbles pseudokinase ortholog nipi-3, is essential for host survival following exposure to P. aeruginosa or ToxA. We find that NIPI-3 mediates the post-developmental expression of intestinal immune genes and proteins and primarily functions in parallel to known immune pathways, including p38 MAPK signaling. Through mutagenesis screening, we identify mutants of the bZIP C/EBP transcription factor cebp-1 that suppress the hypersusceptibility defects of nipi-3 mutants.ConclusionsNIPI-3 is a negative regulator of CEBP-1, which in turn negatively regulates protective immune mechanisms. This pathway represents a previously unknown innate immune signaling pathway in intestinal epithelial cells that is involved in the surveillance of cellular homeostasis. Because NIPI-3 and CEBP-1 are also essential for C. elegans development, NIPI-3 is analogous to other key innate immune signaling molecules such as the Toll receptors in Drosophila that have an independent role during development.Electronic supplementary materialThe online version of this article (doi:10.1186/s12915-016-0334-6) contains supplementary material, which is available to authorized users.

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“…This, in turn, causes an increase in the protein expression of a transcription factor called ZIP-2, which works together with the conserved regulator CEBP-2 to regulate immune responses in C . elegans [ 7 , 8 , 10 ]. The end result is the up-regulation of defense-associated genes via pathways that are required to survive the otherwise lethal effects of this toxin [ 7 – 9 ].…”

Section: Inhibition Of Host Translation Activates a Protective Immunementioning

confidence: 99%

Surveillance Immunity: An Emerging Paradigm of Innate Defense Activation in Caenorhabditis elegans

Pukkila-Worley

2016

PLoS Pathog

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The C. elegans CCAAT-Enhancer-Binding Protein Gamma Is Required for Surveillance Immunity

Cited by 41 publications

References 37 publications

The heat shock response and humoral immune response are mutually antagonistic in honey bees

The heat shock response and humoral immune response are mutually antagonistic in honey bees

Tribbles ortholog NIPI-3 and bZIP transcription factor CEBP-1 regulate a Caenorhabditis elegans intestinal immune surveillance pathway

Surveillance Immunity: An Emerging Paradigm of Innate Defense Activation in Caenorhabditis elegans

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