Deutsch
 
Hilfe Datenschutzhinweis Impressum
  DetailsucheBrowse

Datensatz

DATENSATZ AKTIONENEXPORT
Zur Ablage hinzufügen
  Lokale TagsFreigabegeschichteDetailsÜbersicht

Freigegeben
Zeitschriftenartikel

Parental mutations influence wild-type offspring via transcriptional adaptation

MPG-Autoren
/persons/resource/persons252685

Jiang,  Zhen
Developmental Genetics, Max Planck Institute for Heart and Lung Research, Max Planck Society;

/persons/resource/persons228746

El-Brolosy,  Mohamed A.
Developmental Genetics, Max Planck Institute for Heart and Lung Research, Max Planck Society;

/persons/resource/persons248841

Serobyan,  Vahan
Developmental Genetics, Max Planck Institute for Heart and Lung Research, Max Planck Society;
Department Integrative Evolutionary Biology, Max Planck Institute for Developmental Biology, Max Planck Society;

/persons/resource/persons248845

Welker,  Jordan M.
Developmental Genetics, Max Planck Institute for Heart and Lung Research, Max Planck Society;

/persons/resource/persons248831

Retzer,  Nicholas
Developmental Genetics, Max Planck Institute for Heart and Lung Research, Max Planck Society;

/persons/resource/persons255400

Dooley,  Christopher M.
Developmental Genetics, Max Planck Institute for Heart and Lung Research, Max Planck Society;
Department Genetics, Max Planck Institute for Developmental Biology, Max Planck Society;

/persons/resource/persons251622

Jakutis,  Gabrielius
Developmental Genetics, Max Planck Institute for Heart and Lung Research, Max Planck Society;

Juan,  Thomas
Developmental Genetics, Max Planck Institute for Heart and Lung Research, Max Planck Society;

/persons/resource/persons224231

Fukuda,  Nana
Developmental Genetics, Max Planck Institute for Heart and Lung Research, Max Planck Society;

/persons/resource/persons224247

Maischein,  Hans-Martin
Developmental Genetics, Max Planck Institute for Heart and Lung Research, Max Planck Society;
Department Genetics, Max Planck Institute for Developmental Biology, Max Planck Society;
Research Group Colour Pattern Formation, Max Planck Institute for Developmental Biology, Max Planck Society;

/persons/resource/persons224278

Stainier,  Didier Y. R.
Developmental Genetics, Max Planck Institute for Heart and Lung Research, Max Planck Society;

Externe Ressourcen
Es sind keine externen Ressourcen hinterlegt
Volltexte (beschränkter Zugriff)
Für Ihren IP-Bereich sind aktuell keine Volltexte freigegeben.
Volltexte (frei zugänglich)
Es sind keine frei zugänglichen Volltexte in PuRe verfügbar
Ergänzendes Material (frei zugänglich)
Es sind keine frei zugänglichen Ergänzenden Materialien verfügbar
Zitation

Jiang, Z., El-Brolosy, M. A., Serobyan, V., Welker, J. M., Retzer, N., Dooley, C. M., et al. (2022). Parental mutations influence wild-type offspring via transcriptional adaptation. SCIENCE ADVANCES, 8(47): eabj2029. doi:10.1126/sciadv.abj2029.


Zitierlink: https://hdl.handle.net/21.11116/0000-000D-1C0B-9
Zusammenfassung
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.