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Transposons: catch them if you can

Transposons and their host genomes are entangled in an evolutionary arms race, recounts Tuğçe Aktaş.

Tuğçe Aktaş
Research Highlights09 Mar 2022
Nature Reviews Molecular Cell Biology

Volume: 23, P: 306
De novo mutations in MSL3 cause an X-linked syndrome marked by impaired histone H4 lysine 16 acetylation

De novo mutations in MSL3 cause an X-linked syndrome affecting both males and females. MSL3 mutations reduce H4K16ac levels and lead to misregulation of cellular pathways involved in morphogenesis, cellular shape, and cell migration.

M. Felicia Basilicata
Ange-Line Bruel
Asifa Akhtar
Research17 Sept 2018
Nature Genetics

Volume: 50, P: 1442-1451
Autonomous transposons tune their sequences to ensure somatic suppression

SAFB proteins protect genome integrity by preventing retrotransposition of L1 elements yet maintaining splicing integrity, via prevention of the exonization of previously integrated transposable elements, a major constituent of human genes.

İbrahim Avşar Ilık
Petar Glažar
Tuğçe Aktaş
ResearchOpen Access14 Feb 2024
Nature

Volume: 626, P: 1116-1124
TET activity safeguards pluripotency throughout embryonic dormancy

Here the authors show that active DNA demethylation and transcription factor occupation at distal regulatory elements is essential for pluripotency maintenance in dormancy conditions.

Maximilian Stötzel
Chieh-Yu Cheng
Aydan Bulut-Karslioğlu
ResearchOpen Access23 May 2024
Nature Structural & Molecular Biology

Volume: 31, P: 1625-1639
DHX9 suppresses RNA processing defects originating from the Alu invasion of the human genome

In the absence of DHX9, circular RNAs accumulate and transcription and translation are dysregulated—effects that are exacerbated by concomitant depletion of the RNA-editing enzyme ADAR.

Tuğçe Aktaş
İbrahim Avşar Ilık
Asifa Akhtar
Research29 Mar 2017
Nature

Volume: 544, P: 115-119
Transcriptional and post-transcriptional regulation of transposable elements and their roles in development and disease

Transposable elements (TEs) comprise nearly half of the human genome. This Review discusses transcriptional and post-transcriptional mechanisms that repress TE activity, how TEs escape this suppression and regulate endogenous genes in development and disease, and emerging therapeutic strategies that exploit TE derepression.

İbrahim Avşar Ilık
Xu Yang
Tuğçe Aktaş
Reviews30 Jun 2025
Nature Reviews Molecular Cell Biology

Volume: 26, P: 759-775
A multi-factor trafficking site on the spliceosome remodeling enzyme BRR2 recruits C9ORF78 to regulate alternative splicing

Bergfort et al. use biochemistry, cryoEM, structure-guided mutagenesis, transcriptomics and proteomics to reveal how the intrinsically unstructured C9ORF78 protein binds BRR2 and PRPF8, regulating cassette exons and alternative 3’-splice sites.

Alexandra Bergfort
Marco Preußner
Markus C. Wahl
ResearchOpen Access03 Mar 2022
Nature Communications

Volume: 13, P: 1-16

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Transposons: catch them if you can

De novo mutations in MSL3 cause an X-linked syndrome marked by impaired histone H4 lysine 16 acetylation

Autonomous transposons tune their sequences to ensure somatic suppression

TET activity safeguards pluripotency throughout embryonic dormancy

DHX9 suppresses RNA processing defects originating from the Alu invasion of the human genome

Transcriptional and post-transcriptional regulation of transposable elements and their roles in development and disease

A multi-factor trafficking site on the spliceosome remodeling enzyme BRR2 recruits C9ORF78 to regulate alternative splicing

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Transposons: catch them if you can

De novo mutations in MSL3 cause an X-linked syndrome marked by impaired histone H4 lysine 16 acetylation

Autonomous transposons tune their sequences to ensure somatic suppression

TET activity safeguards pluripotency throughout embryonic dormancy

DHX9 suppresses RNA processing defects originating from the Alu invasion of the human genome

Transcriptional and post-transcriptional regulation of transposable elements and their roles in development and disease

A multi-factor trafficking site on the spliceosome remodeling enzyme BRR2 recruits C9ORF78 to regulate alternative splicing

Search

Quick links