ArticleNature communications2025
Toxoplasma gondii chromatin remodeler SWI/SNF controls parasite division and gene expression.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
1 citing paper in PubMed.
- Two distinct SWI/SNF complexes direct chromatin-linked transcriptional programs in Toxoplasma.Nature communications · 2026Article
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Authors and funding
7 authors.
Funding
Abstract
Toxoplasma gondii is a zoonotic apicomplexan parasite that relies on highly orchestrated gene expression programs to coordinate its cell cycle progression. Although epigenetic mechanisms are recognized as pivotal drivers of developmental gene regulation in parasitic life cycles, the contributions of chromatin remodeling complexes to these processes remain largely unexplored. In this study, we focus on two core ATPase subunits of the SWI/SNF chromatin remodeling complex and investigate their roles in parasite biology and gene regulation. Our findings reveal that these SWI/SNF ATPases work coordinately, occupying the promoters of many tachyzoite-specific genes. Their deletion causes diminished chromatin accessibility and transcriptional reprogramming, downregulating tachyzoite-specific genes and unlocking certain transcripts normally confined to merozoite stage. Loss of these genes severely impairs parasite fitness and causes division defects, with incomplete endopolygeny accompanied by starch accumulation. TgSNF2b also interacts with the MORC remodeler to modulate chromatin architecture and gene expression. These findings provide new insights into the epigenetic regulation of gene expression and cell division in T. gondii and open new avenues for innovative strategies in toxoplasmosis control.
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