Abstract：
:Plasmodium parasites are highly selective when infecting hepatocytes and induce many changes within the host cell upon infection. While several host cell factors have been identified that are important for liver infection, our understanding of what facilitates the maintenance of infection remains incomplete. Here, we describe a role for phosphorylated ribosomal protein S6 (Ser235/236) (p-RPS6) in Plasmodium yoelii-infected hepatocytes. Blocking RPS6 phosphorylation prior to infection decreases the number of liver stage parasites within 24 h. Infected hepatocytes exhibit elevated levels of p-RPS6 while simultaneously abrogating the induction of phosphorylation of RPS6 in response to insulin stimulation. This is in contrast with the regulation of p-RPS6 by Toxoplasma gondii, which elevates levels of p-RPS6 after infection but does not alter the response to insulin. Our data support a model in which RPS6 phosphorylation is uncoupled from canonical regulators in Plasmodium-infected hepatocytes and is relied on by the parasite to maintain infection.
journal_name
Cell Repjournal_title
Cell reportsauthors
Glennon EKK,Austin LS,Arang N,Kain HS,Mast FD,Vijayan K,Aitchison JD,Kappe SHI,Kaushansky Adoi
10.1016/j.celrep.2019.02.085subject
Has Abstractpub_date
2019-03-19 00:00:00pages
3391-3399.e4issue
12issn
2211-1247pii
S2211-1247(19)30271-2journal_volume
26pub_type
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