The gene family encodes ～60 surface antigens by which parasites escape the host immune responses via clonal expression of genes. However， the mechanism controlling this mutual exclusivity， associated with alterations in chromatin assembly， is not understood. Here， we determined how expression of the gene family is regulated by two RecQ DNA helicase family members， PfRecQ1 and PfWRN， in Through genetic manipulation， we found that the complete repertoire was silenced on knockout， whereas their expression did not show noticeable changes when was knocked out. More important， mutually exclusive expression of genes could be rescued by complementation of PfRecQ1. In addition， knocking out... More
The gene family encodes ～60 surface antigens by which parasites escape the host immune responses via clonal expression of genes. However， the mechanism controlling this mutual exclusivity， associated with alterations in chromatin assembly， is not understood. Here， we determined how expression of the gene family is regulated by two RecQ DNA helicase family members， PfRecQ1 and PfWRN， in Through genetic manipulation， we found that the complete repertoire was silenced on knockout， whereas their expression did not show noticeable changes when was knocked out. More important， mutually exclusive expression of genes could be rescued by complementation of PfRecQ1. In addition， knocking out either of these two helicase genes changed the perinuclear cluster distribution of subtelomeres and subtelomeric genes. Whereas deletion of increased the heterochromatin mark trimethylated (H3K9me3) at the transcription start site (TSS) of the gene ， that deletion had no effect on the global distribution of H3K9me3 over gene bodies， including those for the genes. ChIP-seq assay showed that PfRecQ1 was enriched globally at the TSSs of all genes， whereas PfWRN-enriched regions occurred at the gene bodies of the gene family， but not of other genes or at TSSs of all genes. On deletion， the gene moved from the active perinuclear transcription region to a silenced region of the type. These findings imply that PfRecQ1， but not PfWRN， is essential for maintaining the clonal expression of genes.
