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Autonomous transposons tune their sequences to ensure somatic suppression.
İbrahim Avşar Ilık1, Petar Glažar1, Kevin Tse2
1Otto Warburg Laboratories, Max Planck Institute for Molecular Genetics, Berlin, Germany.
Nature
|February 14, 2024
Summary
SAFB proteins prevent transposable elements (TEs) from integrating into the genome and maintain splicing integrity by suppressing TE exonization. This RNA-based defense complements germline pathways, protecting somatic cells from TEs.
Area of Science:
- Genetics
- Molecular Biology
- Epigenetics
Background:
- Transposable elements (TEs) occupy significant portions of genomes, including human introns.
- While transcribed, TEs are typically spliced out and degraded, but can cause splicing errors like exonization.
- A robust splicing code normally prevents TE exonization, but the mechanisms are not fully understood.
Purpose of the Study:
- To investigate the role of SAFB proteins in genome integrity and splicing.
- To understand how SAFB proteins prevent transposable element (TE) exonization.
- To elucidate the broader suppressive activity of SAFB proteins on various repetitive elements.
Main Methods:
- Investigated SAFB protein binding to L1 element sequences.
- Assessed SAFB's impact on splicing of introns containing TEs.
- Examined SAFB's suppressive effects on different types of TEs and genomic elements.
- Compared SAFB expression and activity in somatic cells versus germline cells (testis).
Main Results:
- SAFB proteins bind to adenosine-rich sequences in L1 elements, preventing retrotransposition and TE exonization.
- SAFB's suppressive function extends to cassette exons, nested genes, DNA transposons, and active LTR/ERV elements.
- Splicing events suppressed by SAFB in somatic cells are reactivated in the testis, correlating with low SAFB levels in spermatids.
- SAFB acts as an RNA-based defense system in the soma, distinct from the germline's Piwi-interacting RNA pathway.
Conclusions:
- SAFB proteins play a critical dual role in safeguarding genome integrity by inhibiting TE activity and maintaining splicing fidelity.
- SAFB's mechanism involves direct binding to conserved TE sequences, highlighting a pattern-guided defense strategy.
- SAFB represents a somatic, non-adaptive RNA-based defense against TEs, complementing the adaptive germline RNAi pathways.
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