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Updated: Jun 20, 2026

Investigating Flagella-Driven Motility in Escherichia coli by Applying Three Established Techniques in a Series
Published on: May 10, 2020
Tracking mobilization uncovers an evolutionarily conserved mechanism in suppressing mobile genetic elements
Yi Ni Luo1, Yu Liang2, Shuheng Wu2
1State Key Laboratory of RNA Innovation, Science and Engineering, Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai 200031, China.
Abstract:
Transposons can mobilize within the genome, and these events cause DNA breaks, gene mutations, and genome instability. As such, their aberrant activation is closely linked to cancer, neurodegenerative disorders, and other pathologies. Despite this, the precise mechanisms that suppress transpositions during somatic development remain unclear. Here, by spatiotemporally monitoring transpositions with single-cell resolution, we identified a highly conserved suppression mechanism. We found that Cramp1 plays a critical role in silencing transposon mobility during both Drosophila hindgut regeneration and mouse embryonic erythropoiesis. The function of Cramp1 in controlling transposons is exclusively dependent on linker histone H1-mediated chromatin compaction. Cramp1 specifically binds to DNA sequences within the histone gene cluster, initiating H1 transcription. Subsequently, H1 proteins physically interact with and recruit Nsd to promote the establishment of H3K9 trimethylation (H3K36me2)-modified heterochromatin. Our findings highlight that, in the ongoing evolutionary arms race between hosts and transposons, core mechanisms have evolved to suppress transpositions during somatic development.
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