Evidence map›Paper›PMID 34061407›Full record

ArticleAging cell2021

Oocyte aging is controlled by mitogen-activated protein kinase signaling.

Hanna Achache, Roni Falk, Noam Lerner, Tsevi Beatus, Yonatan B Tzur

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.0field-weighted citation impact, top 7% 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

17 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. NuRD chromatin remodeling is required to repair exogenous DSBs in thebioRxiv : the preprint server for biology · 2025
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Reproductive Aging inFrontiers in cell and developmental biology · 2021
    Review
  16. Aging Negatively Impacts DNA Repair and Bivalent Formation in theFrontiers in cell and developmental biology · 2021
    Article
  17. 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.

Hanna AchacheDepartment of Genetics, Institute of Life Sciences, The Hebrew University of Jerusalem, Jerusalem, Israel.
Roni FalkDepartment of Genetics, Institute of Life Sciences, The Hebrew University of Jerusalem, Jerusalem, Israel.
Noam LernerDepartment of Neurobiology, The Institute of Life Science, The Hebrew University of Jerusalem, Jerusalem, Israel.
Tsevi BeatusDepartment of Neurobiology, The Institute of Life Science, The Hebrew University of Jerusalem, Jerusalem, Israel.
Yonatan B TzurDepartment of Genetics, Institute of Life Sciences, The Hebrew University of Jerusalem, Jerusalem, Israel.ORCID 0000-0002-7715-6113
Hebrew University of Jerusalem · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oogenesis is one of the first processes to fail during aging. In women, most oocytes cannot successfully complete meiotic divisions already during the fourth decade of life. Studies of the nematode Caenorhabditis elegans have uncovered conserved genetic pathways that control lifespan, but our knowledge regarding reproductive aging in worms and humans is limited. Specifically, little is known about germline internal signals that dictate the oogonial biological clock. Here, we report a thorough characterization of the changes in the worm germline during aging. We found that shortly after ovulation halts, germline proliferation declines, while apoptosis continues, leading to a gradual reduction in germ cell numbers. In late aging stages, we observed that meiotic progression is disturbed and crossover designation and DNA double-strand break repair decrease. In addition, we detected a decline in the quality of mature oocytes during aging, as reflected by decreasing size and elongation of interhomolog distance, a phenotype also observed in human oocytes. Many of these altered processes were previously attributed to MAPK signaling variations in young worms. In support of this, we observed changes in activation dynamics of MPK-1 during aging. We therefore tested the hypothesis that MAPK controls oocyte quality in aged worms using both genetic and pharmacological tools. We found that in mutants with high levels of activated MPK-1, oocyte quality deteriorates more rapidly than in wild-type worms, whereas reduction of MPK-1 levels enhances quality. Thus, our data suggest that MAPK signaling controls germline aging and could be used to attenuate the rate of oogenesis quality decline.

Indexed as

AgingAnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsFemaleHumansMitogen-Activated Protein KinasesOocytesSignal TransductionCaenorhabditis elegans ProteinsMitogen-Activated Protein KinasesagingC. elegansfertilityMAPKmeiosisoocyteoogenesis

Identifiers

PMID34061407
PMCPMC8208789
OpenAlexW3165324557

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.