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Genetische und molekulare Analyse euchromatinischer Determinanten der Stilllegung von Transposons in Arabidopsis thaliana

Antragstellerinnen / Antragsteller Professorin Dr. Isabel Bäurle; Dr. Christian Kappel
Fachliche Zuordnung Genetik und Genomik der Pflanzen
Zell- und Entwicklungsbiologie der Pflanzen
Förderung Förderung von 2017 bis 2024
Projektkennung Deutsche Forschungsgemeinschaft (DFG) - Projektnummer 326657501
 
Erstellungsjahr 2022

Zusammenfassung der Projektergebnisse

Transposable elements (TE) pose threats to genome integrity due to their mutagenic activity upon mobilization and transposition. To ensure genome integrity, TEs are subject to epigenetic silencing through DNA methylation and RNA-based mechanisms. We have previously observed in Arabidopsis thaliana that one DNA transposon that is closely linked to a 3’-UTR does not attract silencing, whereas the identical TE is strongly silenced in an intergenic location in a different accession. In this project, we investigated whether TEs escape silencing generally if they are positioned close to protein-coding genes. We have identified TEs with transposition across the Arabidopsis thaliana lineage through computational analysis. Comparing the expression of these TE across accessions, we confirm that TE genes close to genes tend to be more highly expressed than their intergenic homologues. To identify possible regulators of this effect, we explored co-expression between a set of highly-expressed TEs and potential regulators of their expression, including chromatin remodelers, histone modifiers, and RNA processing genes. We identified a cluster with high co-expression across accessions with an exoribonuclease and several nucleosome remodelers, indicating a role for RNA processing and nucleosome organization in opposing epigenetic silencing. Mutants of these genes show reduced expression of the TE cluster, indicating a functional basis for the co-expression. We also find that a histone demethylase that has been reported as an anti-silencing factor for genes next to TEs antagonizes silencing of the highly expressed TEs. In summary, we show that proximity to protein-coding genes generally antagonizes efficient epigenetic silencing, with nucleosome positioning, histone modifications and RNA processing likely playing crucial roles. Future studies will be needed to unravel the molecular details of these anti-silencing activities.

 
 

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