PMK-1 p38 MAPK promotes cadmium stress resistance, the expression of SKN-1/Nrf and DAF-16 target genes, and protein biosynthesis in Caenorhabditis elegans

Keshet, Alex; Mertenskötter, Ansgar; Winter, Sarah; Brinkmann, Vanessa; Dölling, Ramona; Paul, Rüdiger J.

doi:10.1007/s00438-017-1351-z

Cited by 23 publications

(15 citation statements)

References 70 publications

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“…The results in kgb-1 Δ and pmk-1 Δ indicate a higher cadmium sensitivity of pmk-1 Δ. This finding is in accordance with previous results [24], which showed that PMK-1 signaling strongly promotes the cadmium resistance of C. elegans mostly via SKN-1 and DAF-16 target gene expression. Thus, while the cadmium resistance of pmk-1 Δ is impaired by the reduction in DAF-16 target gene expression, there were no specific effects of KGB-1 signaling on DAF-16 activity under hyperosmotic stress [44].…”

Section: Discussionsupporting

confidence: 92%

“…From the data on developmental speed at different cadmium concentrations (Fig. 1a–j), it is evident that a CdCl 2 concentration of 10 mmol/L represents a severe abiotic stress/stressor (see also [24]). With regard to a severe biotic stress/stressor, preliminary experiments in our laboratory suggested to use C. arvensicola as animal feed.…”

Section: Discussionmentioning

confidence: 93%

“…Samples for RNA-Seq (before matrix embedment) were also used for RT-qPCR analyses (see [24] for details). Briefly, RNA concentrations were measured using a NanoDrop spectrophotometer (Thermo Fisher Scientific, Darmstadt, Germany).…”

Section: Methodsmentioning

confidence: 99%

“…Important signaling and processing units for the cellular responses of C. elegans to abiotic or biotic stress are the PMK-1 and KGB-1 mitogen-activated protein kinase (MAPK) and DAF-2 insulin-like signaling pathways. The p38-type PMK-1 MAPK pathway promotes the heat or cadmium resistance of C. elegans [23, 24], with PMK-1 promoting in the latter case also DAF-16-mediated gene expression. PMK-1 signaling is also important for the innate immune response [25, 26, 27] by promoting the expression of immune response genes.…”

Section: Introductionmentioning

confidence: 99%

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Bacterial diet and weak cadmium stress affect the survivability of Caenorhabditis elegans and its resistance to severe stress

Dölling

Mendelski

Paul

2019

Heliyon

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Stress may have negative or positive effects in dependence of its intensity (hormesis). We studied this phenomenon in Caenorhabditis elegans by applying weak or severe abiotic (cadmium, CdCl2) and/or biotic stress (different bacterial diets) during cultivation/breeding of the worms and determining their developmental speed or survival and performing transcriptome profiling and RT-qPCR analyses to explore the genetic basis of the detected phenotypic differences. To specify weak or severe stress, developmental speed was measured at different cadmium concentrations, and survival assays were carried out on different bacterial species as feed for the worms. These studies showed that 0.1 μmol/L or 10 mmol/L of CdCl2 were weak or severe abiotic stressors, and that E. coli HT115 or Chitinophaga arvensicola feeding can be considered as weak or severe biotic stress. Extensive phenotypic studies on wild type (WT) and different signaling mutants (e.g., kgb-1Δ and pmk-1Δ) and genetic studies on WT revealed, inter alia, the following results. WT worms bred on E. coli OP50, which is a known cause of high lipid levels in the worms, showed high resistance to severe abiotic stress and elevated gene expression for protein biosynthesis. WT worms bred under weak biotic stress (E. coli HT115 feeding which causes lower lipid levels) showed an elevated resistance to severe biotic stress, elevated gene expression for the innate immune response and signaling but reduced gene expression for protein biosynthesis. WT worms bred under weak biotic and abiotic stress (E. coli HT115 feeding plus 0.1 μmol/L of CdCl2) showed high resistance to severe biotic stress, elevated expression of DAF-16 target genes (e.g., genes for small heat shock proteins) but further reduced gene expression for protein biosynthesis. WT worms bred under weak biotic but higher abiotic stress (E. coli HT115 feeding plus 10 μmol/L of CdCl2) showed re-intensified gene expression for the innate immune response, signaling, and protein biosynthesis, which, however, did not caused a higher resistance to severe biotic stress. E. coli OP50 feeding as well as weak abiotic and biotic stress during incubations also improved the age-specific survival probability of adult WT worms. Thus, this study showed that a bacterial diet resulting in higher levels of energy resources in the worms (E. coli OP50 feeding) or weak abiotic and biotic stress promote the resistance to severe abiotic or biotic stress and the age-specific survival probability of WT.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 93%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Bacterial diet and weak cadmium stress affect the survivability of Caenorhabditis elegans and its resistance to severe stress

Dölling

Mendelski

Paul

2019

Heliyon

Self Cite

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“…Many candidate antimicrobial genes have been identified in the genome of C. elegans ; but the role of the signaling pathways in regulating these antimicrobial peptides in response to bacterial infection is yet to be fully elucidated ( 40 – 42 ). In the present study, four genes ( tir-1, nsy-1, sek-1 , and pmk-1 ) in the p38 MAPK pathway, two genes ( daf-16 and age-1 ) in the DAF/IGF pathway, six genes ( lys-7, spp-1, abf-2, clec-85 , and clec-60 , and abf-3 ) reported previously that encode antimicrobial peptides ( 27 ), and three other genes ( sod-3, dbl-1 , and skn-1 ) reported previously with a defense function ( 23 , 43 , 44 ) were initially examined for their possible involvement in the immune response of the wild-type nematode. All the tested genes except for tir-1, clec-60 , and skn-1 were upregulated significantly as the results of responding to ETEC infection (Figure 2 ).…”

Section: Discussionmentioning

confidence: 97%

Cell Signaling of Caenorhabditis elegans in Response to Enterotoxigenic Escherichia coli Infection and Lactobacillus zeae Protection

Zhou

Liu

et al. 2018

Front. Immunol.

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Enterotoxigenic Escherichia coli (ETEC) infection causes the death of Caenorhabditis elegans, which can be prevented by certain Lactobacillus isolates. The host response of C. elegans to ETEC infection and its regulation by the isolates are, however, largely unclear. This study has revealed that, in agreement with the results of life-span assays, the expression of the genes encoding p38 mitogen-activated protein kinase (MAPK) pathway (nsy-1, sek-1, and pmk-1), insulin/insulin-like growth factor (DAF/IGF) pathway (daf-16), or antimicrobial peptides (lys-7, spp-1, and abf-3) and other defensing molecules (abf-2, clec-85) was upregulated significantly when the wild-type nematode (N2) was subjected to ETEC infection. This upregulation was further enhanced by the pretreatment with Lactobacillus zeae LB1, but not with L. casei CL11. Mutants defective in the cell signaling of C. elegans were either more susceptible (defective in NSY-1, SEK-1, PMK-1, or DAF16) or more resistant (defective in AGE-1, DBL-1, SKN-1, or SOD-3) to ETEC infection compared with the wild-type. Mutants defective in antimicrobial peptides (LYS-7, SPP1, or ABF-3) were also more susceptible. In addition, mutants that are defective in NSY-1, SEK-1, PMK-1, DAF16, ABF-3, LYS-7, or SPP1 showed no response to the protection from L. zeae LB1. The expression of the genes encoding antimicrobial peptides (lys-7, spp-1, and abf-3) and other defensing molecules (abf-2, clec-60, and clec-85) were almost all upregulated in AGE-1- or DBL-1-defective mutant compared with the wild-type, which was further enhanced by the pretreatment of L. zeae LB1. The expression of these genes was, however, mostly downregulated in NSY-1- or DAF-16-defective mutant. These results suggest that L. zeae LB1 regulates C. elegans signaling through the p38 MAPK and DAF/IGF pathways to control the production of antimicrobial peptides and defensing molecules to combat ETEC infection.

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Cadmium-induced oxidative stress, histopathology, and transcriptomic changes in the hepatopancreas of Fenneropenaeus merguiensis

Ju,

Ndandala,

Lei

et al. 2024

Aquaculture Reports

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PMK-1 p38 MAPK promotes cadmium stress resistance, the expression of SKN-1/Nrf and DAF-16 target genes, and protein biosynthesis in Caenorhabditis elegans

Cited by 23 publications

References 70 publications

Bacterial diet and weak cadmium stress affect the survivability of Caenorhabditis elegans and its resistance to severe stress

Bacterial diet and weak cadmium stress affect the survivability of Caenorhabditis elegans and its resistance to severe stress

Cell Signaling of Caenorhabditis elegans in Response to Enterotoxigenic Escherichia coli Infection and Lactobacillus zeae Protection

Cadmium-induced oxidative stress, histopathology, and transcriptomic changes in the hepatopancreas of Fenneropenaeus merguiensis

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