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Influence of p38 MAPK (PMK-1) on the heat stress response of C. elegans

ABSTRACT: PMK-1 is involved in the heat stress response of C. elegans, translocates to the nucleus upon heat exposure and influences the expression of chaperone genes, proteasomal subunits and protein-biosynthesis related genes.

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE41205 | GEO | 2012/11/05

SECONDARY ACCESSION(S): PRJNA176153

REPOSITORIES: GEO

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Influence of p38 MAPK (PMK-1) on the heat stress response of C. elegans

Project description:PMK-1 is involved in the heat stress response of C. elegans, translocates to the nucleus upon heat exposure and influences the expression of chaperone genes, proteasomal subunits and protein-biosynthesis related genes. Differential Gene expression of WT and pmk-1 deletion mutant (KU25) after 5 hours at 35Â°C

2012-11-05 | E-GEOD-41205 | biostudies-arrayexpress

Analysis of PMK-1 p38 MAPK and PMK-1(D327E) Caspase Cleavage Resistant Mutant and Effect of DAF-16 (FOXO) Mutants on Gene Regulation in C. elegans

Project description:We identified genes inversely regulated by pmk-1 null mutation and pmk-1(D327E). We also identified genes working through daf-16, working around daf-16 and working independent of daf-16

2022-07-12 | GSE192941 | GEO

Analyses of CED-3 caspase and PMK-1 p38 MAPK in gene regulation in C elegans

Project description:We identified more than 300 genes inversely regulated by ced-3 and pmk-1 that enriched for epidermal stress response factors in C elegans

2020-05-01 | GSE145983 | GEO

The p38 MAPK PMK-1 shows heat-induced nuclear translocation, supports chaperone expression, and affects the heat tolerance of Caenorhabditis elegans.

Project description:The p38 mitogen-activated protein kinase PMK-1 of Caenorhabditis elegans has been associated with heavy metal, oxidative and pathogen stress. Pmk-1 is part of an operon comprising three p38 homologues, with pmk-1 expression suggested to be regulated by the operon promoter. There are contradictory reports about the cellular localization of PMK-1. We were interested to study principles of pmk-1 expression and to analyze the role of PMK-1 under heat stress. Using a translational GFP reporter, we found pmk-1 expression to be driven by a promoter in front of pmk-1. PMK-1 was detected in intestinal cells and neurons, with a cytoplasmic localization at moderate temperature. Increasing temperature above 32 °C, however, induced a nuclear translocation of PMK-1 as well as PMK-1 accumulation near to apical membranes. Testing survival rates revealed 34-35 °C as critical temperature range, where short-term survival severely decreased. Mutants of the PMK-1 pathway (pmk-1Δ, sek-1Δ, mek-1Δ) as well as a mutant of JNK pathway (jnk-1Δ) showed significantly lower survival rates than wild-type or mutants of other pathways (kgb-1Δ, daf-2Δ). Rescue and overexpression experiments verified the negative effects of pmk-1Δ on heat tolerance. Studying gene expression by RNA-seq and semi-quantitative reverse transcriptase polymerase chain reaction revealed positive effects of the PMK-1 pathway on the expression of genes for chaperones, protein biosynthesis, protein degradation, and other functional categories. Thus, the PMK-1 pathway is involved in the heat stress responses of C. elegans, possibly by a PMK-1-mediated activation of the transcription factor SKN-1 and/or an indirect or direct PMK-1-dependent activation (hyperphosphorylation) of heat-shock factor 1.

| S-EPMC3631094 | biostudies-literature

Metformin promotes innate immunity through a conserved PMK-1/p38 MAPK pathway.

Project description:Metformin, as the first-line oral drug for type 2 diabetes, has proven benefits against aging, cancer and cardiovascular diseases. But the influence of metformin to the immune response and its molecular mechanisms remain obscure. Metformin increases resistance to not only the Gram-negative pathogens Pseudomonas aeruginosa and Salmonella enterica but also the Gram-positive pathogens Enterococcus faecalis and Staphylococcus aureus. Meanwhile, metformin protects the animals from the infection by enhancing the tolerance to the pathogen infection rather than by reducing the bacterial burden. Through the screening of classical immune pathways in C. elegans, we find metformin enhances innate immunity through p38 MAPK pathway. Furthermore, activated p38/PMK-1 by metformin acts on the intestine for innate immune response. In addition, metformin-treated mice have increased resistance to P. aeruginosa PA14 infection and significantly increased the levels of active PMK-1. Therefore, promoted p38/PMK-1-mediated innate immunity by metformin is conserved from worms to mammals. Our work provides a conserved mechanism by which metformin enhances immune response and boosts its therapeutic application in the treatment of pathogen infection.

| S-EPMC6961722 | biostudies-literature

Muscleblind Splicing Factor Regulates Longevity Through p38 MAPK Signaling

Project description:Muscleblind-like splicing regulators (MBNLs) are RNA-binding factors that have an important role in developmental processes. Dysfunction of these factors is a key contributor of different neuromuscular degenerative disorders, including Myotonic Dystrophy type 1 (DM1). Since DM1 is a multisystemic disease characterized by symptoms resembling accelerated aging, we asked which cellular processes do MBNLs regulate that make them necessary for normal lifespan. By utilizing the model organism Caenorhabditis elegans, we found that loss of MBL-1 (the sole ortholog of mammalian MBNLs), which is known to be required for normal lifespan, shortens lifespan by decreasing the activity of p38 MAPK/PMK-1 as well as the function of transcription factors ATF-7 and SKN-1. Furthermore, we show that mitochondrial stress caused by knockdown of mitochondrial electron transport chain components promotes the longevity of mbl-1 mutants in a partially PMK-1-dependent manner. Together, the data establish a mechanism of how DM1-associated loss of muscleblind affects lifespan. Furthermore, this study suggests that mitochondrial stress could alleviate symptoms caused by the dysfunction of muscleblind splicing factor, creating a potential approach to investigate for therapy.

2021-07-20 | GSE146801 | GEO

Analyses of CED-3 caspase and PMK-1 p38 MAPK in gene regulation in C elegans

Project description:Analyses of CED-3 caspase and PMK-1 p38 MAPK in gene regulation in C elegans

| PRJNA608907 | ENA

Analysis of PMK-1 p38 MAPK and PMK-1(D327E) Caspase Cleavage Resistant Mutant and Effect of DAF-16 (FOXO) Mutants on Gene Regulation in C. elegans

Project description:Analysis of PMK-1 p38 MAPK and PMK-1(D327E) Caspase Cleavage Resistant Mutant and Effect of DAF-16 (FOXO) Mutants on Gene Regulation in C. elegans

| PRJNA793860 | ENA

Genes regulated by PMK-1 and DAF-16 in a daf-2(e1368) background.

Project description:Analysis of genes differentially expressed between daf-2(e1368) and daf-2(e1368);pmk-1(km25) and between daf-2(e1368) and daf-2(e1368);daf-16(mgDf47). These studies identified genes upregulated by wild-type PMK-1 and wild-type DAF-16. Keywords: genetic modification

2007-02-08 | GSE5801 | GEO

Exercise suppresses mouse systemic AApoAII amyloidosis through enhancement of the p38 MAPK signaling pathway

Project description:Exercise interventions are beneficial for reducing the risk of age-related diseases, including amyloidosis, but the underlying molecular links remain unelucidated. Here, we investigated the protective role of interval exercise training in a mouse model of age-related systemic apolipoprotein A-II amyloidosis (AApoAII) and elucidated potential mechanisms. Mice subjected to sixteen weeks of exercise improved whole-body physiologic functions and exhibited substantial inhibition of amyloidosis, particularly in the liver and spleen. Exercise activated the hepatic p38 mitogen-activated protein kinase (p38 MAPK) signaling pathway and the downstream transcription factor tumor suppressor p53. This activation resulted in elevated expression and phosphorylation of heat shock protein beta-1 (HSPB1), a chaperone that defends against protein aggregation. In the amyloidosis-induced mice, the hepatic p38 MAPK-related adaptive responses were additively enhanced by exercise. We observed that with exercise, greatly increased amounts of phosphorylated HSPB1 accumulated at amyloid deposition areas, which we suspect to inhibit amyloid fibril formation. Collectively, our findings conclude exercise-activated, specific chaperone prevention of amyloidosis, and suggest that exercise may amplify intracellular stress-related protective adaptation pathways against age-associated disorders such as amyloidosis.

2022-03-04 | GSE192521 | GEO

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