English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Background  Invasion of the mosquito salivary glands by  Plasmodium  is a critical step for malaria transmission. From a SAGE analysis, we previously identified several genes whose expression in salivary glands was regulated coincident with sporozoite invasion of salivary glands. To get insights into the consequences of these salivary gland responses, here we have studied one of the genes,  PRS1  ( Plasmodium responsive salivary 1 ), whose expression was upregulated in infected glands, using immunolocalization and functional inactivation approaches.    Methodology/Principal Findings    PRS1  belongs to a novel insect superfamily of genes encoding proteins with DM9 repeat motifs of uncharacterized function. We show that  PRS1  is induced in response to  Plasmodium , not only in the salivary glands but also in the midgut, the other epithelial barrier that  Plasmodium  has to cross to develop in the mosquito. Furthermore, this induction is observed using either the rodent parasite  Plasmodium berghei  or the human pathogen  Plasmodium falciparum . In the midgut, PRS1 overexpression is associated with a relocalization of the protein at the periphery of invaded cells. We also find that sporozoite invasion of salivary gland cells occurs sequentially and induces intra-cellular modifications that include an increase in  PRS1  expression and a relocalization of the corresponding protein into vesicle-like structures. Importantly,  PRS1  knockdown during the onset of midgut and salivary gland invasion demonstrates that  PRS1  acts as an agonist for the development of both parasite species in the two epithelia, highlighting shared vector/parasite interactions in both tissues.    Conclusions/Significance  While providing insights into potential functions of DM9 proteins, our results reveal that PRS1 likely contributes to fundamental interactions between  Plasmodium  and mosquito epithelia, which do not depend on the specific  Anopheles / P. falciparum  coevolutionary history.

Anopheles Gambiae PRS1 Modulates Plasmodium Development at Both Midgut and Salivary Gland Steps