Knockdown of proteins involved in iron metabolism limits tick reproduction and development
Jazyk angličtina Země Spojené státy americké Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
19171899
PubMed Central
PMC2633537
DOI
10.1073/pnas.0807961106
PII: 0807961106
Knihovny.cz E-zdroje
- MeSH
- analýza přežití MeSH
- biologické modely MeSH
- ferritin genetika MeSH
- fylogeneze MeSH
- hmyzí geny MeSH
- hmyzí proteiny genetika metabolismus MeSH
- intracelulární prostor metabolismus MeSH
- klíšťata genetika růst a vývoj fyziologie MeSH
- klonování DNA MeSH
- messenger RNA genetika metabolismus MeSH
- morčata MeSH
- proteosyntéza MeSH
- regulace genové exprese MeSH
- rozmnožování MeSH
- stanovení celkové genové exprese MeSH
- stravovací zvyklosti MeSH
- umlčování genů MeSH
- western blotting MeSH
- železo metabolismus MeSH
- zvířata MeSH
- Check Tag
- morčata MeSH
- mužské pohlaví MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- ferritin MeSH
- hmyzí proteiny MeSH
- messenger RNA MeSH
- železo MeSH
Ticks are among the most important vectors of a wide range of human and animal diseases. During blood feeding, ticks are exposed to an enormous amount of free iron that must be appropriately used and detoxified. However, the mechanism of iron metabolism in ticks is poorly understood. Here, we show that ticks possess a complex system that efficiently utilizes, stores and transports non-heme iron within the tick body. We have characterized a new secreted ferritin (FER2) and an iron regulatory protein (IRP1) from the sheep tick, Ixodes ricinus, and have demonstrated their relationship to a previously described tick intracellular ferritin (FER1). By using RNA interference-mediated gene silencing in the tick, we show that synthesis of FER1, but not of FER2, is subject to IRP1-mediated translational control. Further, we find that depletion of FER2 from the tick plasma leads to a loss of FER1 expression in the salivary glands and ovaries that normally follows blood ingestion. We therefore suggest that secreted FER2 functions as the primary transporter of non-heme iron between the tick gut and the peripheral tissues. Silencing of the fer1, fer2, and irp1 genes by RNAi has an adverse impact on hatching rate and decreases postbloodmeal weight in tick females. Importantly, knockdown of fer2 dramatically impairs the ability of ticks to feed, thus making FER2 a promising candidate for development of an efficient anti-tick vaccine.
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