Dataset Information

Dynamics of Transposable Element Invasions with piRNA Clusters.

ABSTRACT: In mammals and invertebrates, the proliferation of an invading transposable element (TE) is thought to be stopped by an insertion into a piRNA cluster. Here, we explore the dynamics of TE invasions under this trap model using computer simulations. We found that piRNA clusters confer a substantial benefit, effectively preventing extinction of host populations from a proliferation of deleterious TEs. TE invasions consist of three distinct phases: first, the TE amplifies within the population, next TE proliferation is stopped by segregating cluster insertions, and finally the TE is inactivated by fixation of a cluster insertion. Suppression by segregating cluster insertions is unstable and bursts of TE activity may yet occur. The transposition rate and the population size mostly influence the length of the phases but not the amount of TEs accumulating during an invasion. Solely, the size of piRNA clusters was identified as a major factor influencing TE abundance. We found that a single nonrecombining cluster is more efficient in stopping invasions than clusters distributed over several chromosomes. Recombination among cluster sites makes it necessary that each diploid carries, on the average, four cluster insertions to stop an invasion. Surprisingly, negative selection in a model with piRNA clusters can lead to a novel equilibrium state, where TE copy numbers remain stable despite only some individuals in a population carrying a cluster insertion. In Drosophila melanogaster, the trap model accounts for the abundance of TEs produced in the germline but fails to predict the abundance of TEs produced in the soma.

SUBMITTER: Kofler R

PROVIDER: S-EPMC6573471 | biostudies-literature | 2019 Jul

REPOSITORIES: biostudies-literature

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Dynamics of Transposable Element Invasions with piRNA Clusters.

Kofler Robert R

Molecular biology and evolution 20190701 7

In mammals and invertebrates, the proliferation of an invading transposable element (TE) is thought to be stopped by an insertion into a piRNA cluster. Here, we explore the dynamics of TE invasions under this trap model using computer simulations. We found that piRNA clusters confer a substantial benefit, effectively preventing extinction of host populations from a proliferation of deleterious TEs. TE invasions consist of three distinct phases: first, the TE amplifies within the population, next ...[more]

PMID: 30968135

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Project description:Transposable elements (TE) are selfish genetic elements that can cause harmful mutations. In Drosophila, it has been estimated that half of all spontaneous visible marker phenotypes are mutations caused by TE insertions. Several factors likely limit the accumulation of exponentially amplifying TEs within genomes. First, synergistic interactions between TEs that amplify their harm with increasing copy number are proposed to limit TE copy number. However, the nature of this synergy is poorly understood. Second, because of the harm posed by TEs, eukaryotes have evolved systems of small RNA-based genome defense to limit transposition. However, as in all immune systems, there is a cost of autoimmunity and small RNA-based systems that silence TEs can inadvertently silence genes flanking TE insertions. In a screen for essential meiotic genes in Drosophila melanogaster, a truncated Doc retrotransposon within a neighboring gene was found to trigger the germline silencing of ald, the Drosophila Mps1 homolog, a gene essential for proper chromosome segregation in meiosis. A subsequent screen for suppressors of this silencing identified a new insertion of a Hobo DNA transposon in the same neighboring gene. Here we describe how the original Doc insertion triggers flanking piRNA biogenesis and local gene silencing. We show that this local gene silencing occurs in cis and is dependent on deadlock, a component of the Rhino-Deadlock-Cutoff (RDC) complex, to trigger dual-strand piRNA biogenesis at TE insertions. We further show how the additional Hobo insertion leads to de-silencing by reducing flanking piRNA biogenesis triggered by the original Doc insertion. These results support a model of TE-mediated gene silencing by piRNA biogenesis in cis that depends on local determinants of transcription. This may explain complex patterns of off-target gene silencing triggered by TEs within populations and in the laboratory. It also provides a mechanism of sign epistasis among TE insertions, illuminates the complex nature of their interactions and supports a model in which off-target gene silencing shapes the evolution of the RDC complex.

Dataset Information

Dynamics of Transposable Element Invasions with piRNA Clusters.

Publications

Dynamics of Transposable Element Invasions with piRNA Clusters.

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