Abstract
Transposable elements are common targets for transcriptional and post-transcriptional gene silencing in eukaryotic genomes. However, the molecular mechanisms responsible for sensing such repeated sequences in the genome remain largely unknown. Here, we show that machinery of homologous recombination (HR) and RNA silencing play cooperative roles in copy number-dependent de novo DNA methylation of the retrotransposon MAGGY in the fungus Pyricularia oryzae. Genetic and physical interaction studies revealed that RecA domain-containing proteins, including P. oryzae homologs of Rad51, Rad55, and Rad57, together with an uncharacterized protein, Ddnm1, form complex(es) and mediate either the overall level or the copy number-dependence of de novo MAGGY DNA methylation, likely in conjunction with DNA repair. Interestingly, P. oryzae mutants of specific RNA silencing components (MoDCL1 and MoAGO2) were impaired in copy number-dependence of MAGGY methylation. Co-immunoprecipitation of MoAGO2 and HR components suggested a physical interaction between the HR and RNA silencing machinery in the process.
Highlights
Transposable elements are common targets for transcriptional and post-transcriptional gene silencing in eukaryotic genomes
We first determined whether MGY-ΔRT, a transposition-deficient MAGGY mutant having a 513-bp deletion in the reversetranscriptase domain[14], is targeted for de novo DNA methylation in a MAGGY-free P. oryzae isolate (Br48)
They are transcriptionally suppressed by heterochromatin formation and post-transcriptionally silenced by RNAi and/or its related pathways
Summary
Transposable elements are common targets for transcriptional and post-transcriptional gene silencing in eukaryotic genomes. Chemical modifications of chromatin components, such as histone hypoacetylation, methylation of histone H3 at lysine 9 or 27, and DNA methylation, are associated with heterochromatin formation in a wide range of organisms[2,3] Repetitive sequences, such as transposable elements (TEs), are common targets for heterochromatin formation, which contributes to the maintenance of genome integrity by suppressing deleterious transpositions and chromosomal recombination between repetitive elements. The results show that the RecA domain-containing HR components such as P. oryzae homologs of Rad[51], Rad[55], and Rad[57] participates in copy number-dependent de novo methylation of MAGGY, possibly through a RNA-directed DNA methylation (RdDM)-like pathway This suggests that HR and heterochromatin formation against retrotransposons could share molecular machinery for repeat search at least in part
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