Evidence map›Paper›PMID 36427314›Full record

ArticleScience advances2022

Parental mutations influence wild-type offspring via transcriptional adaptation.

Zhen Jiang, Mohamed A El-Brolosy, Vahan Serobyan, Jordan M Welker, Nicholas Retzer, Christopher M Dooley, Gabrielius Jakutis, Thomas Juan, Nana Fukuda, Hans-Martin Maischein and 2 more

Open access · goldAbstract read
In one paragraph

Article in Science advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

9 citing papers in PubMed, 16 citations in OpenAlex.

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  6. Modelling Lowe syndrome and Dent-2 disease using zebrafish.Frontiers in cell and developmental biology · 2025
    Review
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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

12 authors at 2 institutions in 3 countries.

Zhen Jiang *Max Planck Institute for Heart and Lung Research, Department of Developmental Genetics, Bad Nauheim, Germany.ORCID 0000-0003-3648-8549
Mohamed A El-Brolosy *Max Planck Institute for Heart and Lung Research, Department of Developmental Genetics, Bad Nauheim, Germany.ORCID 0000-0003-2433-1851
Vahan Serobyan *Max Planck Institute for Heart and Lung Research, Department of Developmental Genetics, Bad Nauheim, Germany.ORCID 0000-0001-5055-8422
Jordan M WelkerMax Planck Institute for Heart and Lung Research, Department of Developmental Genetics, Bad Nauheim, Germany.ORCID 0000-0003-1017-9449
Nicholas RetzerMax Planck Institute for Heart and Lung Research, Department of Developmental Genetics, Bad Nauheim, Germany.
Christopher M DooleyMax Planck Institute for Heart and Lung Research, Department of Developmental Genetics, Bad Nauheim, Germany.
Gabrielius JakutisMax Planck Institute for Heart and Lung Research, Department of Developmental Genetics, Bad Nauheim, Germany.ORCID 0000-0002-1311-5742
Thomas JuanMax Planck Institute for Heart and Lung Research, Department of Developmental Genetics, Bad Nauheim, Germany.ORCID 0000-0002-9654-3717
Nana FukudaMax Planck Institute for Heart and Lung Research, Department of Developmental Genetics, Bad Nauheim, Germany.
Hans-Martin MaischeinMax Planck Institute for Heart and Lung Research, Department of Developmental Genetics, Bad Nauheim, Germany.
Darius BalciunasDepartment of Biology, College of Science and Technology, Temple University, Philadelphia, PA, USA.ORCID 0000-0003-1938-3243
Didier Y R StainierMax Planck Institute for Heart and Lung Research, Department of Developmental Genetics, Bad Nauheim, Germany.ORCID 0000-0002-0382-0026
Max Planck Institute for Heart and Lung Research · DEVilnius University · LT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transgenerational epigenetic inheritance (TEI) is mostly discussed in the context of physiological or environmental factors. Here, we show intergenerational and transgenerational inheritance of transcriptional adaptation (TA), a process whereby mutant messenger RNA (mRNA) degradation affects gene expression, in nematodes and zebrafish. Wild-type offspring of animals heterozygous for mRNA-destabilizing alleles display increased expression of adapting genes. Notably, offspring of animals heterozygous for nontranscribing alleles do not display this response. Germline-specific mutations are sufficient to induce TA in wild-type offspring, indicating that, at least for some genes, mutations in somatic tissues are not necessary for this process. Microinjecting total RNA from germ cells of TA-displaying heterozygous zebrafish can trigger TA in wild-type embryos and in their progeny, suggesting a model whereby mutant mRNAs in the germline trigger a TA response that can be epigenetically inherited. In sum, this previously unidentified mode of TEI reveals a means by which parental mutations can modulate the offspring's transcriptome.

Indexed as

AcclimatizationZebrafishAnimalsHeterozygoteMutationRNA, MessengerRNA, Messenger

Identifiers

PMID36427314
PMCPMC9699682
OpenAlexW4309958350

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.