MIC11 Removal Traps Toxoplasma Inside Host Cells
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- University of Osaka researchers used an in vivo CRISPR-based screen to identify the MIC11 gene as essential for Toxoplasma gondii egress from host cells, avoiding limitations of past in vitro screens that opened host cells during screening.
- MIC11 deletion prevented Toxoplasma gondii parasites from rupturing the host cell membrane, trapping them inside host cells and disrupting the parasite life cycle.
- Lead author Yuta Tachibana stated the in vivo screen identified for the first time that MIC11 is essential for host cell membrane permeabilization and parasite egress.
- Senior author Masahiro Yamamoto reported evidence that MIC11 interacts with PLP1, a parasite protein already known to be essential for egress, providing further evidence of MIC11's crucial role.
- Toxoplasma gondii has felines (both domestic and wild) as definitive hosts where it sexually reproduces, and infects nearly all warm-blooded mammals as intermediate hosts for asexual reproduction.
- The findings could guide development of novel treatments for parasite-borne diseases such as toxoplasmosis and malaria, per the researchers, with the paper published in Nature Communications.
Why it matters: Past studies on parasite egress genes produced conflicting results because in vitro screens opened host cells, making it impossible to reliably detect egress-blocking mutations; the new in vivo approach from University of Osaka overcomes that limitation and identifies MIC11 as a specific drug target for disrupting the Toxoplasma life cycle.
