Evidence map›Paper›PMID 41120898›Full record

ArticleBMC genomics2025

The chromatin remodeler LET-418/Mi-2 regulates the intracellular pathogen response in the C. elegans intestine.

Shweta Rajopadhye, Vladimir Lažetić, David Rodriguez-Crespo, Emily Troemel, Peter Meister, Chantal Wicky

Abstract read
In one paragraph

Article in BMC genomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Shweta RajopadhyeDepartment of Biology, University of Fribourg, Fribourg, Switzerland.
Vladimir LažetićDepartment of Biological Sciences, Columbian College of Arts and Sciences, The George Washington University, District of Columbia, Washington, USA.
David Rodriguez-CrespoDepartment of Biology, University of Fribourg, Fribourg, Switzerland.
Emily TroemelSchool of Biological Sciences, University of California, San Diego, La Jolla, CA, USA.
Peter MeisterInstitute of Cell Biology, University of Bern, Bern, Switzerland.
Chantal WickyDepartment of Biology, University of Fribourg, Fribourg, Switzerland. chantal.wicky@unifr.ch.

Funding

The Intracellular Pathogen Response Triggers Defense Against Co-evolved PathogensR01GM114139 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Emily R Troemel · 2015 to 2026
$3.1M
Probing organismal proteostasis through the response to intracellular infectionR01AG052622 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Emily R Troemel · 2017 to 2026
$2.7M
Innate immunity against viral infection in intestinal epithelial cells of C. elegansR01AI176639 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Emily R Troemel · 2023 to 2026
$1.5M
NIAID NIH HHS R01 AI176639NIA NIH HHS R01 AG052622NIGMS NIH HHS R01 GM114139Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung IZCOZ0_198093
6 · The paper itself

Abstract

Chromatin remodeling provides essential transcriptional regulation for all biological processes. In Caenorhabditis elegans, the chromatin remodeler LET-418, a homolog of the human Mi-2β protein, plays a critical role in regulating development, organogenesis, tissue maintenance, stress resistance and lifespan. LET-418 is part of several chromatin remodeling complexes and contributes significantly to the balance between growth and defense mechanisms, yet its target genes remain unclear. Using DNA methylation profiling, we identified genomic binding sites and associated target genes of LET-418 and its MEC-complex-specific interactor MEP-1 in the intestine. Consistent with their presence in the same complex, the two proteins shared more than half of their target genes. Functional analysis revealed that LET-418 and MEP-1 target genes are highly active in the intestine and are involved in repressing innate immune responses, including the intracellular pathogen response (IPR). Consistently, in let-418 mutants, IPR-induced genes, such as pals-5 or pals-2 are strongly upregulated, in a manner dependent on ZIP-1, a major transcription factor for IPR. Additionally, we found pathogen levels of the natural intracellular intestinal pathogen Nematocida parisii significantly reduced in let-418 mutants, supporting the observation of increased IPR in this mutant. Altogether, these findings reveal a crucial role for LET-418 as a modulator of the IPR, aligning with its role in maintaining the balance between development and defense.

Indexed as

Caenorhabditis elegansCaenorhabditis elegans ProteinsChromatin Assembly and DisassemblyIntestinesAnimalsDNA MethylationGene Expression RegulationImmunity, InnateIntestinal MucosaMutationTranscription FactorsCaenorhabditis elegans ProteinsTranscription Factors

Identifiers

PMID41120898
PMCPMC12538751

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.