BackgroundLarvae of the tapeworm E. multilocularis cause alveolar echinococcosis (AE), one of the most lethal helminthic infections in humans. A population of stem cell-like cells, the germinative cells, is considered to drive the larval growth and development within the host. The molecular mechanisms controlling the behavior of germinative cells are largely unknown.Methodology/Principal findingsUsing in vitro cultivation systems we show here that the EGFR/ERK signaling in the parasite can promote germinative cell proliferation in response to addition of human EGF, resulting in stimulated growth and development of the metacestode larvae. Inhibition of the signaling by either the EGFR inhibitors CI-1033 and BIBW2992 or the MEK/ERK inhibitor U0126 impairs germinative cell proliferation and larval growth.Conclusions/SignificanceThese data demonstrate the contribution of EGF-mediated EGFR/ERK signaling to the regulation of germinative cells in E. multilocularis, and suggest the EGFR/ERK signaling as a potential therapeutic target for AE and perhaps other human cestodiasis.
Background
Secreted effector proteins play critical roles in plant-fungal interactions. The
Magnaporthe oryzae
genome encodes a large number of secreted proteins. However, the function of majority of
M. oryzae
secreted proteins remain to be characterized. We previously identified 851 in planta-expressed
M. oryzae
genes encoding putative secreted proteins, and characterized five
M. oryzae
cell death–inducing proteins MoCDIP1 to MoCDIP5. In the present study, we expand our work on identification of novel MoCDIP proteins.
Results
We performed transient expression assay of 98 more in planta-expressed
M. oryzae
putative secreted protein genes, and identified eight novel proteins, MoCDIP6 to MoCDIP13, that induced plant cell death. Yeast secretion assay and truncation expression analysis revealed that the signal peptides that led the secretion of proteins to the extracellular space, were required for cell death inducing activity of the novel MoCDIPs except for MoCDIP8. Exogenous treatment of rice seedlings with recombinant MoCDIP6 or MoCDIP7 resulted in enhanced resistance to blast fungus, indicating that the two MoCDIPs trigger cell death and elicit defense responses in rice.
Conclusions
The newly identified MoCDIP6 to MoCDIP13, together with previously identified MoCDIP1 to MoCDIP5, provide valuable targets for further dissection of the molecular mechanisms underlying the rice-blast fungus interaction.
Electronic supplementary material
The online version of this article (10.1186/s12284-019-0312-z) contains supplementary material, which is available to authorized users.
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