Evidence map›Paper›PMID 19923212›Full record

ArticleThe Journal of biological chemistry2010

The Caenorhabditis elegans germ line regulates distinct signaling pathways to control lifespan and innate immunity.

Scott Alper, Matthew K McElwee, Javier Apfeld, Brad Lackford, Jonathan H Freedman, David A Schwartz

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
1.3field-weighted citation impact, top 23% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

47 citing papers in PubMed, 75 citations in OpenAlex.

  1. Article
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  4. SICKO: Systematic Imaging ofbioRxiv : the preprint server for biology · 2024
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Immunosenescence in Caenorhabditis elegans.Immunity & ageing : I & A · 2022
    Article
  10. Article
  11. Article
  12. Article
  13. Article
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  15. Review
  16. Review
  17. Aiweixin, a Traditional Uyghur Medicinal Formula, Extends the Lifespan ofEvidence-based complementary and alternative medicine : eCAM · 2019
    Article
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 2 countries.

Scott AlperIntegrated Department of Immunology, National Jewish Health, Denver, Colorado 80206, USA. alpers@njhealth.org
Matthew K McElwee
Javier Apfeld
Brad Lackford
Jonathan H Freedman
David A Schwartz
National Institutes of Health · USNational Jewish Health · USHarvard University · US

Funding

Comparative Genomic Responses to Environmental StressorsZIAES102045 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI FREEDMAN, JONATHAN H · 2009 to 2014
$6.9M
Intramural NIH HHS
6 · The paper itself

Abstract

The relationship between the mechanisms that control an organism's lifespan and its ability to respond to environmental challenges are poorly understood. In Caenorhabditis elegans, an insulin-like signaling pathway modulates lifespan and the innate immune response to bacterial pathogens via a common mechanism involving transcriptional regulation by the DAF-16/FOXO transcription factor. The C. elegans germ line also modulates lifespan in a daf-16-dependent manner. Here, we show that the germ line controls the innate immune response of C. elegans somatic cells to two different Gram-negative bacteria. In contrast to the insulin-like signaling pathway, the germ line acts via distinct signaling pathways to control lifespan and innate immunity. Under standard nematode culture conditions, the germ line regulates innate immunity in parallel to a known p38 MAPK signaling pathway, via a daf-16-independent pathway. Our findings indicate that a complex regulatory network integrates inputs from insulin-like signaling, p38 MAPK signaling, and germ line stem cells to control innate immunity in C. elegans. We also confirm that innate immunity and lifespan in C. elegans are distinct processes, as nonoverlapping regulatory networks control survival in the presence of pathogenic and nonpathogenic bacteria. Finally, we demonstrate that the p38 MAPK pathway in C. elegans is activated to a similar extent by both pathogenic and nonpathogenic bacteria, suggesting that both can induce the nematode innate immune response.

Indexed as

Immunity, InnateLongevitySignal TransductionAnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsForkhead Transcription FactorsGene Expression RegulationGerm CellsGlucagon-Like Peptide 1Mitogen-Activated Protein KinasesMutationp38 Mitogen-Activated Protein KinasesPhosphorylationPseudomonas aeruginosaSerratia marcescensCaenorhabditis elegans Proteinsdaf-16 protein, C elegansForkhead Transcription FactorsGlucagon-Like Peptide 1Mitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein KinasesPmk-1 protein, C elegansTranscription Factors

Identifiers

PMID19923212
PMCPMC2804340
OpenAlexW1973928364

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.