Abstract
The opportunistic pathogen Toxoplasma gondii is highly adept at manipulating host cell functions. While inside a host cell, Toxoplasma divides within a parasitophorous vacuole from which it secretes numerous effector proteins from its dense granules. Many of these so-called GRA proteins are translocated from the parsitophorous vacuole into the host cell where they directly disrupt host signaling pathways. The machinery that drives the translocation of GRA proteins across the parasitophorous vacuole membrane is being elucidated through both genetic and biochemical approaches. A new mSphere research article (M. W. Panas, A. Ferrel, A. Naor, E. Tenborg, et al., mSphere 4:e00276-19, 2019, https://doi.org/10.1128/mSphere.00276-19) describes how the kinase ROP17, which is secreted from the parasite's rhoptries into the host cell during invasion, regulates the translocation of GRA effectors.
Highlights
Toxoplasma gondii is an obligate intracellular parasite with the remarkable ability to infect any nucleated cell in virtually all warm-blooded animals
While some of these GRA proteins stay within the parasitophorous vacuole (PV) space or associate with the PV membrane (PVM), some of them, such as GRA16, GRA18, and GRA24, are translocated across the PVM into the host cytosol where they affect various host cell signaling pathways
In a new report in mSphere (5), Panas et al describe how the rhoptry serine/threonine kinase ROP17, which is secreted during invasion and associates with the host cytosol side of the PV, is required for translocation of GRA effectors and the ensuing host
Summary
Toxoplasma gondii is an obligate intracellular parasite with the remarkable ability to infect any nucleated cell in virtually all warm-blooded animals. KEYWORDS GRA16, GRA24, MYR1, ROP17, Toxoplasma gondii, c-MYC, effectors, kinase, protein translocation Part of its success as a parasite and pathogen are due to a large arsenal of effectors that are secreted into the host cell during invasion and intracellular growth (1).
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