Enterovirus 71 (EV71) is a highly transmissible pathogenic agent that causes severe central nervous system diseases in infected infants and young children. Here, we reported that EV71 VP1 protein could bind to vimentin intermediate filaments expressed on the host cell surface. Soluble vimentin or an antibody against vimentin could inhibit the binding of EV71 to host cells. Accompanied with the reduction of vimentin expression on the cell surface, the binding of EV71 to cells was remarkably decreased. Further evidence showed that the N terminus of vimentin is responsible for the interaction between EV71 and vimentin. These results indicated that vimentin on the host cell surface may serve as an attachment site that mediated the initial binding and subsequently increased the infectivity of EV71.
IMPORTANCEThis study delivers important findings on the roles of vimentin filaments in relation to EV71 infection and provides information that not only improves our understanding of EV71 pathogenesis but also presents us with potentially new strategies for the treatment of diseases caused by EV71 infections.
Potassium antimonate was used to localize Ca 2+ in tobacco ovules from 0 to 7 d after anthesis in pollinated and emasculated flowers. Antimonate binds ''loosely bound'' Ca 2+ into calcium antimonate; lesssoluble forms are unavailable and free calcium usually escapes. Ovules are immature at anthesis. Abundant calcium precipitates in nucellar cells surrounding the micropylar canal. A difference between calcium in the two synergids emerges at 1 d, which is enhanced in pollinated flowers. The future receptive synergid accumulates more precipitates in the nucleus, cytoplasm and cell walls. After fertilization, micropyle precipitates diminish, and the ovule is unreceptive to further tube entry. In emasculated flowers 6 d after anthesis, ovular precipitates essentially disappear; however, flowers pollinated at 4-5 d and collected 2 d later largely restore their prior concentration of precipitates. Ovular precipitates occur initially in the nucellus, then the embryo sac, and finally the synergid and micropylar filiform apparatus. Possibility, calcium is released from the embryo sac, although no structural evidence of exudate formation was observed. Calcium precipitates in the ovule correlate with the ability of the ovule to be fertilized, suggesting that successful pollen tube entry and later development may require calcium of the class precipitated by antimonate.Abbreviations: EDXA = energy-dispersive X-ray analysis; ES = embryo Sac; ppt = precipitate Correspondence
Some plant and animal pathogens can manipulate their hosts to cause them to release odors that are attractive to the pathogens' arthropod vectors. However, the molecular mechanism underlying this process is largely unexplored, and the specific effectors the pathogens employ as well as the pathways within the hosts they target are currently unknown. Here we reveal that the aphid-borne cucumber mosaic virus (CMV) employs its 2b protein, a well-characterized viral suppressor of host RNA interference (VSR), to target the host's jasmonate (JA) hormone pathway, thus acting as a viral inducer of host attractiveness to insect vectors (VIA). 2b inhibits JA signaling by directly interacting with and repressing JA-induced degradation of host jasmonate ZIM-domain proteins, instead of using its VSR activity. Our findings identify a previously defined VSR protein as a VIA and uncover a molecular mechanism CMV uses to manipulate host's attractiveness to insect vectors by targeting host hormone signaling.
The study investigated the antifungal activity and potential antifungal mechanisms of volatile compounds (i.e., E‐2‐hexenal) against Penicillium cyclopium, one of the main tomato postharvest pathogens, which was obtained and purified from postharvest tomato surface. Experimental data suggested that the volatile compound exhibited strong antifungal activity against the targeted pathogens, with minimum inhibitory concentration and minimum fungicidal concentration of 160 μL/L and 320μL/L for E‐2‐hexenal, respectively. The membrane permeability of the P. cyclopium increased with increasing concentrations of E‐2‐hexenal, as evidenced by cell constituent release, leakage of potassium ions, and extracellular conductivity. Moreover, E‐2‐hexenal could induce a decrease in total lipid content and extracellular pH. These results suggest that the anti‐fungal activity of E‐2‐hexenal against P. cyclopium can be attributed to the disruption of the cell membrane integrity, the increase of membrane permeability and the leakage of cell components.
Practical Applications
Penicillium cyclopium was isolated from the surface of tomato fruits after harvest. E‐2‐hexenal had an inhibitory effect on the hyphae and spores of P. cyclopium. The minimum inhibitory concentration and minimum fungicidal concentration were determined by using different concentrations of E‐2‐hexenal against P. cyclopium. The study results indicate that the antifungal activity of E‐2‐hexenal against P. cyclopium can be attributed to the disruption of the cell membrane integrity, the increase of membrane permeability and the leakage of cell components. The study results provided a reference for extending the storage of tomato fruits.
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