GSE208560
Patterns of heterochromatin distribution alterations linked to transcriptional changes at Plasmodium falciparum clonally variant gene loci [ChIP-seq]
The survival of malaria parasites in the changing human blood environment largely depends on their ability to alter gene expression by epigenetic mechanisms. The active state of Plasmodium falciparum clonally variant genes is associated with euchromatin characterized by the histone mark H3K9ac, whereas the silenced state is characterized by H3K9me3-based heterochromatin. However, the localization of the euchromatin-heterochromatin transitions associated with expression switches in different clonally variant genes has not been characterized. Here we compared the distribution of heterochromatin between subclones of the same genetic background with different patterns of expressed and silenced clonally variant genes to identify at a genome-wide level the patterns associated with the different transcriptional states. We found that de novo heterochromatin formation or complete disruption of a heterochromatin domain are relatively rare events, and in the majority of loci expression switches can be explained by expansion or retraction of heterochromatin. We describe different modalities of heterochromatin changes linked to transcriptional differences, revealing a complex scenario. Despite this complexity, heterochromatin distribution patterns generally enable prediction of the transcriptional state of clonally variant genes. Some subclones expressed and had in an active chromatin state several var genes simultaneously. We also found that heterochromatin levels in the putative regulatory region of the gdv1-as non-coding RNA, previously involved in sexual commitment, varied between parasite lines with different sexual conversion rates. Overall design: Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for histonemodifications H3K9me3 and H3K9ac in different P.Falciparum strains/subclones.