Evidence map›Paper›PMID 26196144›Full record

ArticleeLife2015

Lipid-mediated regulation of SKN-1/Nrf in response to germ cell absence.

Michael J Steinbaugh, Sri Devi Narasimhan, Stacey Robida-Stubbs, Lorenza E Moronetti Mazzeo, Jonathan M Dreyfuss, John M Hourihan, Prashant Raghavan, Theresa N Operaña, Reza Esmaillie, T Keith Blackwell

Open access · goldAbstract read
In one paragraph

Article in eLife, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 140 papers.

0numbers the graph read from it
0cells of the map it votes in
140citing papers in PubMed
7.9field-weighted citation impact, top 2% 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

140 citing papers in PubMed, 227 citations in OpenAlex.

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  5. LIN-23 AffectsbioRxiv : the preprint server for biology · 2026
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80 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Michael J SteinbaughResearch Division, Joslin Diabetes Center, Boston, United States.ORCID http://orcid.org/0000-0002-2403-2221
Sri Devi NarasimhanResearch Division, Joslin Diabetes Center, Boston, United States.
Stacey Robida-StubbsResearch Division, Joslin Diabetes Center, Boston, United States.
Lorenza E Moronetti MazzeoResearch Division, Joslin Diabetes Center, Boston, United States.
Jonathan M DreyfussResearch Division, Joslin Diabetes Center, Boston, United States.
John M HourihanDepartment of Genetics and Harvard Stem Cell Institute, Harvard Medical School, Boston, United States.
Prashant RaghavanResearch Division, Joslin Diabetes Center, Boston, United States.
Theresa N OperañaResearch Division, Joslin Diabetes Center, Boston, United States.
Reza EsmaillieResearch Division, Joslin Diabetes Center, Boston, United States.
T Keith BlackwellResearch Division, Joslin Diabetes Center, Boston, United States.
Joslin Diabetes Center · USBoston University · US

Funding

SPECIAL ASSAY COREP30DK036836 · NIDDK · JOSLIN DIABETES CENTER · PI JEAN E. SCHAFFER · 1986 to 2026
$50.5M
TRAINING IN DIABETES AND METABOLISMT32DK007260 · NIDDK · JOSLIN DIABETES CENTER · PI LAURIE J GOODYEAR · 1986 to 2026
$13.6M
Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Ann E. Rougvie · 2012 to 2026
$7.5M
SKN-1 Regulation and Oxidative Stress Resistance in C. elegansR01GM062891 · NIGMS · JOSLIN DIABETES CENTER · PI BLACKWELL, T KEITH · 2001 to 2016
$5.6M
Regulation of C. elegans SKN-1/Nrf activity by the unfolded protein responseR01GM094398 · NIGMS · JOSLIN DIABETES CENTER · PI BLACKWELL, T KEITH · 2012 to 2015
$1.2M
Regulation of SKN-1/Nrf functions by germline stem cellsR21AG043949 · NIA · JOSLIN DIABETES CENTER · PI BLACKWELL, T KEITH · 2013 to 2014
$456k
NIA NIH HHS R21 AG043949NIA NIH HHS R21AG043949NIDDK NIH HHS P30 DK036836NIDDK NIH HHS P30DK036836NIDDK NIH HHS T32 DK007260NIDDK NIH HHS T32DK007260NIGMS NIH HHS R01 GM062891NIGMS NIH HHS R01GM062891NIGMS NIH HHS R01 GM094398NIGMS NIH HHS R01GM094398NIH HHS P40 OD010440
6 · The paper itself

Abstract

In Caenorhabditis elegans, ablation of germline stem cells (GSCs) extends lifespan, but also increases fat accumulation and alters lipid metabolism, raising the intriguing question of how these effects might be related. Here, we show that a lack of GSCs results in a broad transcriptional reprogramming in which the conserved detoxification regulator SKN-1/Nrf increases stress resistance, proteasome activity, and longevity. SKN-1 also activates diverse lipid metabolism genes and reduces fat storage, thereby alleviating the increased fat accumulation caused by GSC absence. Surprisingly, SKN-1 is activated by signals from this fat, which appears to derive from unconsumed yolk that was produced for reproduction. We conclude that SKN-1 plays a direct role in maintaining lipid homeostasis in which it is activated by lipids. This SKN-1 function may explain the importance of mammalian Nrf proteins in fatty liver disease and suggest that particular endogenous or dietary lipids might promote health through SKN-1/Nrf.

Indexed as

Gene Expression RegulationLipid MetabolismAnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsDNA-Binding ProteinsGerm CellsTranscription FactorsCaenorhabditis elegans ProteinsDNA-Binding Proteinsskn-1 protein, C elegansTranscription FactorsagingC. eleganscell biologychromosomesfatty acid signalinggenesgermline stem cellslipid metabolismproteostasisSKN-1/Nrf

Identifiers

PMID26196144
PMCPMC4541496
OpenAlexW2160395555

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.