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Post‐transcriptional silencing of UIS4 in P lasmodium berghei sporozoites is important for host switch
Author(s) -
Silvie Olivier,
Briquet Sylvie,
Müller Katja,
Manzoni Giulia,
Matuschewski Kai
Publication year - 2014
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/mmi.12528
Subject(s) - biology , plasmodium berghei , microbiology and biotechnology , gene silencing , infectivity , open reading frame , plasmodium (life cycle) , untranslated region , rna interference , parasite hosting , messenger rna , virology , gene , genetics , rna , malaria , immunology , peptide sequence , virus , world wide web , computer science
Summary P lasmodium sporozoites are transmitted by mosquitoes and first infect hepatocytes of their mammalian host, wherein they develop as liver stages, surrounded by the parasitophorous vacuole membrane ( PVM ). The parasite must rapidly adapt to its changing environment after switching host. Shortly after invasion, the PVM is remodelled by insertion of essential parasite proteins of the early transcribed membrane protein family such as UIS 4. Here, using the rodent malaria model P lasmodium berghei , we show that transcripts encoding UIS 4 are stored in a translationally repressed state in sporozoites, allowing UIS 4 protein synthesis only after host cell invasion. Using a series of reporter transgenic parasite lines we could demonstrate that the open reading frame of UIS4 mRNA is critical for gene silencing, whereas the 5′ and 3′ untranslated regions are dispensable. Our data further indicate that the UIS4 translational repression machinery is present only in mature sporozoites in the mosquito salivary glands, and that premature expression of UIS 4 protein results in a loss of parasite infectivity. Our findings reveal the importance of specific post‐transcriptional control in sporozoites, and establish that host switch requires high levels of translationally silent UIS4 RNA , which permits stage conversion, yet avoids premature expression of this liver stage‐specific protein.