Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1263103 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR33576263_1.fastq.gz | Fastqsanger.gz | |||
| SRR33576263_2.fastq.gz | Fastqsanger.gz | |||
| SRR33576264_1.fastq.gz | Fastqsanger.gz | |||
| SRR33576264_2.fastq.gz | Fastqsanger.gz | |||
| SRR33576265_1.fastq.gz | Fastqsanger.gz |
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Project description:Host-derived factors are sucked into midgut of mosquitoes during natural malaria transmission, but their influence on malaria transmission is largely unknown. We reported that mouse complement C3 taken into mosquitoes significantly promoted malaria transmission either in laboratory or in field. This effect was attributed to the reduction of microbiota abundance in mosquito midgut by host-derived C3 through direct lyses the predominant symbiont bacteria Elizabethkingia anopheles. Elizabethkingia anopheles symbiont bacteria were demonstrated to be detrimental to malaria sexual stages in mosquitoes. Strikingly, the promoted effect of host C3 on malaria transmission was confirmed by laboratory mosquitoes membrane-feeding on Plasmodium falciparum. Therefore, we reveal a novel strategy of malaria parasite to utilize host complement C3 to promote its transmission, and the administration of C3 inhibitor would provide us a novel strategy to control malaria transmission.
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Project description:Transcriptional responses in the gut of the main malaria vector Anopheles gambiae following oral bacterial infection with the entomopathogen Serratia marcescens were identified using DNA microarrays. S. marcescens is a common member of the mosquito gut microbiota, found in both laboratory reared and field collected mosquitoes, that can be potentially pathogenic as in Drosophila (Nehme et al., 2007), while it has been shown to influence the outcome of Plasmodium infections (Bando et al., 2013). S. marcescens belongs to the Enterobacteriaceae family, members of which have been shown to influence malaria transmission dynamics (Cirimotich et al., 2011, Boissiere et al., 2012). To further investigate the interactions between S. marcescens and the mosquito host, likely to shape, directly or indirectly, malaria transmission dynamics, An. gambiae mosquitoes, from the recently established N'gousso M form laboratory colony that retains much of the genetic variation of field mosquitoes, were antibiotic treated for 5 days and subsequently orally infected with the Db11-GFP strain of S. marcescens. Bacteria-fed mosquitoes were selected 2 days post infection, and, 3 days post infection, guts from bacteria-fed mosquitoes were dissected. Uninfected control mosquitoes were treated in the same way. Differential expression in the gut of S. marcescens infected mosquitoes, compared to uninfected controls, was identified by hybridizing labelled complementary RNA, derived from total RNA extracted from the respective gut pools, in customized Agilent 4x44k gene expression microarrays, comprising oligonucleotide probes encompassing all An. gambiae annotated genes of the AgamP3.6 release, with each probe represented in duplicate.
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Project description:Protein phosphorylation plays a critical role during the development of malaria parasites. Here, we performed a functional analysis of the Plasmodium berghei Ser/Thr protein phosphatase 6 (PbPP6), which was associated with the plasma membrane of macrogametes and ookinetes. Compared to wild-type P. berghei, genetic disruption/deletion of the pbpp6 gene (∆pbpp6) reduced the asexual growth of the parasites and prolonged the survival of ∆pbpp6-infected mice. The ∆pbpp6 parasites showed impaired gametogenesis, particularly affecting male gametogenesis, which substantially decreased ookinete formation and transmission to mosquitoes. RNA-seq assays revealed that pbpp6 disruption led to over 11-fold down-regulation of the nek3 gene, a regulator of MAPK2 in the PKG-Ca2+ signaling cascade during male gametogenesis. Several PDEs (α, γ, δ) were also affected, indicating that PbPP6 plays a role in the cGMP-PKG-Ca2+ signaling pathway. Additionally, we observed altered expression of messenger ribonucleoproteins in the Δpbpp6 parasites, which may affect translational repression of stored mRNAs in female gametocytes and post-fertilization development in mosquitoes. Consistent with the dysregulated GO terms related to the cGMP-PKG-Ca2+ signaling cascade observed in RNA-seq analysis, the activated gametocytes of ∆pbpp6 exhibited significantly reduced levels of intracellular cGMP, cytosolic Ca2+ mobilization, and DNA replication. Phosphoproteomic analysis detected increased phosphorylation at the Ser508 site of guanylyl cyclase alpha (GCα), suggesting that PbPP6 regulates cGMP-PKG-Ca2+ signaling cascades by modulating the activity of GCα during gametogenesis. This study highlights the potential of targeting PP6 to disrupt malaria transmission.
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Project description:Plasmodium falciparum is a unicellular parasite responsible for the majority of 440,000 death due to malaria every year. Due to their essential role for malaria transmission, gametocytes represent prime targets for transmission-blocking strategies intended to prevent spread of the deadly disease. In this study, we explored the signaling pathways leading to gametogenesis and identified a hitherto unknown protein, which structurally belongs to the class of seven-helix proteins and which thus was termed 7-helix-1. The protein is specifically expressed in female gametocytes and gene disruption leads to impaired gamete formation and thus reduced transmission of malaria parasites to mosquitoes. The loss of 7-helix-1 caused significant changes in the expression of components of the molecular machinery needed by eukaryotic cells to synthesize proteins. We thus propose that 7-helix-1 is a key regulator needed to coordinate the increased need of proteins at the onset of gametogenesis.
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