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Trends Parasitol. 2017 Dec;33(12):947-960. doi: 10.1016/j.pt.2017.08.006. Epub 2017 Sep 20.

Translational Control in the Latency of Apicomplexan Parasites.

Author information

1
Department of Pharmacology and Toxicology, Indiana University School of Medicine, Indianapolis, IN, USA; Department of Biochemistry & Molecular Biology, Indiana University School of Medicine, Indianapolis, IN, USA.
2
Department of Pharmacology and Toxicology, Indiana University School of Medicine, Indianapolis, IN, USA; Department of Biochemistry & Molecular Biology, Indiana University School of Medicine, Indianapolis, IN, USA; Department of Pediatrics, Indiana University School of Medicine, Indianapolis, IN, USA.
3
Department of Biochemistry & Molecular Biology, Indiana University School of Medicine, Indianapolis, IN, USA.
4
Department of Pharmacology and Toxicology, Indiana University School of Medicine, Indianapolis, IN, USA; Departments of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN, USA. Electronic address: wjsulliv@iu.edu.

Abstract

Apicomplexan parasites Toxoplasma gondii and Plasmodium spp. use latent stages to persist in the host, facilitate transmission, and thwart treatment of infected patients. Therefore, it is important to understand the processes driving parasite differentiation to and from quiescent stages. Here, we discuss how a family of protein kinases that phosphorylate the eukaryotic initiation factor-2 (eIF2) function in translational control and drive differentiation. This translational control culminates in reprogramming of the transcriptome to facilitate parasite transition towards latency. We also discuss how eIF2 phosphorylation contributes to the maintenance of latency and provides a crucial role in the timing of reactivation of latent parasites towards proliferative stages.

KEYWORDS:

Plasmodium; Toxoplasma; eIF2; latency; translational control

PMID:
28942109
PMCID:
PMC5705472
[Available on 2018-12-01]
DOI:
10.1016/j.pt.2017.08.006
[Indexed for MEDLINE]

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