Authors

R Augusto²; D Roquis³; A Taudt⁴; K Geyer¹; G Padalino¹; K F Hoffmann¹; N Holroyd⁶; M Berriman⁶; B Aliaga⁵; C Chaparro²; C Grunau⁵;  ¹ Aberystwyth University, UK;  ² IHPE, France;  ³ IRHS, France;  ⁴ University of Groningen, Netherlands;  ⁵ University of Perpignan via Domitia, France;  ⁶ Wellcome Trust Sanger Institute, UK

Discussion

Schistosoma mansoni is a parasitic flatworm and causative agent of intestinal schistosomiasis, a neglected tropical disease affecting 67 million people worldwide. The parasite has a complex life cycle involving two obligate consecutive hosts (a cold-blooded snail and a warm-blooded mammal). We show here that the chromatin structure of five different developmental stages is characterized by specific changes in posttranslational histone modifications, in particular methylation of H3K4, H3K27 and H4K20. E.g. bivalent methylation in H3K4me3 and H3K27me3 at transcription start sites (TSS) of genes is a landmark of cercaria. In addition to specific modifications around genes, repetitive sequences undergo characteristic changes in their chromatin structure during the lifecycle. Trimethylation of H3K27 at TSS is found in sporocysts and pharmacological inhibition of G9a/GLP and EZH2 histone methyltransferase orthologs in S. mansoni efficiently blocked miracidia to sporocyst transition. Consequently, histone methylation emerges as suitable target for control of schistosomiasis.