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<p>Genomes constantly face threats from transposable elements (TEs) and other genomic parasites. While the silencing of existing TE has been well studied, little is known about how cells recognize new invading TEs that they have not previously encountered. Here we explore this question by inserting foreign sequences into <i>S. pombe</i>. Our data revealed that the newly invading TE <i>tj1</i> is recognized and targeted for silencing by RNAi and heterochromatin. The efficiency of recognition, as well as the degree and stability of silencing, depends on the copy number and insertion location of the TE. We demonstrated that RNA, rather than DNA, is sensed, and that the efficiency of TE recognition correlates with levels of RNA antisense to the TE, generated from upstream transcripts. We also show that various genes of non-transposable nature can initiate silencing. Our data show that silencing may not require recognition of specific elements in the transposon by the host defense systems, and suggest that disruption of host transcription patterns triggers recognition of TE.</p>

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Recognition and silencing of a new transposable element

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年5月22日

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  • Luca Salvi,
  • Yinxia Yan,
  • Mario Halic

摘要

Genomes constantly face threats from transposable elements (TEs) and other genomic parasites. While the silencing of existing TE has been well studied, little is known about how cells recognize new invading TEs that they have not previously encountered. Here we explore this question by inserting foreign sequences into S. pombe. Our data revealed that the newly invading TE tj1 is recognized and targeted for silencing by RNAi and heterochromatin. The efficiency of recognition, as well as the degree and stability of silencing, depends on the copy number and insertion location of the TE. We demonstrated that RNA, rather than DNA, is sensed, and that the efficiency of TE recognition correlates with levels of RNA antisense to the TE, generated from upstream transcripts. We also show that various genes of non-transposable nature can initiate silencing. Our data show that silencing may not require recognition of specific elements in the transposon by the host defense systems, and suggest that disruption of host transcription patterns triggers recognition of TE.