Evidence map›Paper›PMID 36176234›Full record

ArticleAging cell2022

Meiotic dysfunction accelerates somatic aging in Caenorhabditis elegans.

Julia A Loose, Francis R G Amrit, Thayjas Patil, Judith L Yanowitz, Arjumand Ghazi

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.7field-weighted citation impact, top 36% 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

5 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. 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

5 authors at 1 institution in 1 country.

Julia A LooseDepartment of Pediatrics, John G. Rangos Sr. Research Center, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.
Francis R G AmritDepartment of Pediatrics, John G. Rangos Sr. Research Center, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.
Thayjas PatilDepartment of Pediatrics, John G. Rangos Sr. Research Center, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.
Judith L YanowitzDepartment of Obstetrics, Gynecology, and Reproductive Sciences, Magee-Womens Research Institute, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
Arjumand GhaziDepartment of Pediatrics, John G. Rangos Sr. Research Center, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.ORCID 0000-0002-5859-4206
University of Pittsburgh · US

Funding

Undergraduate Summer Research Supplement for 5R01GM104007-07: Characterization of a Meiotic Crossover Surveillance SystemR01GM104007 · NIGMS · MAGEE-WOMEN'S RES INST AND FOUNDATION · PI YANOWITZ, JUDITH L · 2013 to 2021
$2.6M
The Coordination of Lipid Synthesis and Breakdown in Metabolism and AgingR01AG051659 · NIA · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GHAZI, ARJUMAND · 2016 to 2019
$1.6M
Role of the transcription elongation and splicing factor TCER-1 in repressing immunity and promoting fertilityR56AG066682 · NIA · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GHAZI, ARJUMAND · 2021 to 2021
$321k
COELOMOCYTES IN C.ELEGANS--CELL FATE DETERMINATIONF32HD008715 · NICHD · CARNEGIE INSTITUTION OF WASHINGTON, D.C. · PI YANOWITZ, JUDITH L · 2000 to 2002
$112k
NIA NIH HHS R01 AG051659NIA NIH HHS R56 AG066682NICHD NIH HHS F32 HD008715NIGMS NIH HHS R01 GM104007
6 · The paper itself

Abstract

An expanding body of evidence, from studies in model organisms to human clinical data, reveals that reproductive health influences organismal aging. However, the impact of germline integrity on somatic aging is poorly understood. Moreover, assessing the causal relationship of such an impact is challenging to address in human and vertebrate models. Here, we demonstrate that disruption of meiosis, a germline restricted process, shortened lifespan, impaired individual aspects of healthspan, and accelerated somatic aging in Caenorhabditis elegans. Young meiotic mutants exhibited transcriptional profiles that showed remarkable overlap with the transcriptomes of old worms and shared similarities with transcriptomes of aging human tissues as well. We found that meiosis dysfunction caused increased expression of functionally relevant longevity determinants whose inactivation enhanced the lifespan of normal animals. Further, meiotic mutants manifested destabilized protein homeostasis and enhanced proteasomal activity partially rescued the associated lifespan defects. Our study demonstrates a role for meiotic integrity in controlling somatic aging and reveals proteostasis control as a potential mechanism through which germline status impacts overall organismal health.

Indexed as

Caenorhabditis elegansCaenorhabditis elegans ProteinsAgingAnimalsGerm CellsHumansLongevityCaenorhabditis elegans ProteinsagingC. elegansgerm cellsgermlinehealthspanlifespanmeiosisproteostasisreproductionsoma-germline signaling

Identifiers

PMID36176234
PMCPMC9649607
OpenAlexW4298089024

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.