ArticlePLoS pathogens2026
Schistosoma japonicum histone acetyltransferase 1 (SjHAT1): A novel anti-schistosomal drug target.
Article in PLoS pathogens, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Schistosomiasis remains a critical global health issue, necessitating novel therapies due to emerging praziquantel resistance. We previously developed a patented praziquantel derivative, DW-3-15, which demonstrated potent broad-spectrum schistosomicidal activity through SjHAT1 inhibition. Here, the full-length SjHAT1 cDNA is cloned by rapid amplification of cDNA ends methods. The protein encoded by the cDNA retains conserved catalytic residues of acetyltransferases although sharing 34% identity with mammalian orthologs. Enzyme activity analysis reveals that recombinant SjHAT1 exhibits 130 μU/mL histone acetyltransferase activity at 25°C for 60 min, and is completely inhibited by DW-3-15 at a concentration of 50 μM. However, DW-3-15 has no effect on the enzymatic activity of the human ortholog HAT1. Phylogenetic analyses place SjHAT1 in a distinct clade, and molecular docking results indicate significant divergence compared to its human ortholog HsHAT1. The expression profiling of SjHAT1 reveals stage- and sex-specific patterns. Fluorescence in situ hybridization localizes SjHAT1 predominantly in female vitellaria and male parenchyma near the gynecophoral canal. Knockdown of SjHAT1 reduces worm survival by 57.5% in vivo, suppresses female oviposition by 90.8% in vitro and 79.2% in vivo, and disrupts ovarian and vitelline architecture. RNA-sequencing analysis reveals that SjHAT1 knockdown disrupts β-alanyl-tryptamine (BATT) pheromone signaling via downregulation of aromatic L-amino acid decarboxylase (AADC) in males and multidrug resistance-associated protein 4 (MRP4) in females. Given that BATT is essential for inducing female sexual development and egg production, the observed transcriptional dysregulation provides mechanistic evidence for disrupted intersexual communication. Our findings identify that SjHAT1 is a central regulator of schistosome reproductive biology. These sex-specific mechanisms highlight SjHAT1 as a potential therapeutic target for treatment and control of schistosomiasis.
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