1967 Volume 33 Issue 4 Pages 244-252
Chenopodium sap used mainly in this study was the supernatant from centrifuged (9, 000×g, 20min.) leaf homogenate with three fold (by weight) of 0.2M phosphate buffer solution (pH 6.0), avoiding cold acetone soluble parts, being dialyzed against water, and was designated ChIS. To test the inhibitory effect of Chenopodium sap on the infection of non-persistent virus, daikon mosaic virus (DMV) (the Japanese strain of turnip mosaic virus) and its local lesion host, White Burley tobacco were mainly used. Experiments were carried out by abrasion with virus diseased plant sap and also with Chenopodium sap on the half leaves of the lesion host. Inhibitory effect was shown with the percentages obtained by the comparison of the lesion number on treated half leaves with that on the opposite half leaves (controls).1) No decline of inhibitory effect on virus infection of Chenopodium sap heated at 60°C for 10 minutes was observed; while the effect lost when the sap was heated at 100°C for 10 minutes (Table 1, 2, and 3). 2) Inhibitory effect fell remarkably when rubbed with DMV on its original plant, Chenopodium album (Table 4). 3) No inhibitory effect on DMV infection was obtained when DMV was inoculated on upper side of a tobacco leaf soon after its under side was rubbed with ChIS (Table 5). 4) Efficacy of inhibition of ChIS on DMV infection was observed with a 1 to 100 dilution (Fig. 1). Further dilution of the sap resulted remarkable fall of inhibitory effect. 5) Efficacy of inhibition of ChIS on DMV infection was observed even when rubbed 48 hours before the virus inoculation (Table 6). 6) As to after application of ChIS, efficacy of the inhibiting sap on DMV infection was observed up to 30 minutes after the virus inoculation. 7) No inhibitory effect of ChIS on DMV infection was observed when tobacco leaves were syringed or rubbed with ChIS before inoculation of the virus with Myzus persicae (Table 7). 8) No inhibitory effect of ChIS on DMV infection was again observed when tobacco leaves were rubbed with ChIS after inoculation of the virus with M. persicae by brief feeding period of 15 to 20 seconds (Table 8 and 9).
To explain the mechanism of the inhibiting action against virus infection of the inhibitor such as Chenopodium sap, the idea that the inhibitor acts on the host cytoplasm and inhibits the formation of virus-receptor complex is now widely accepted.
In addition to this a working hypothesis, “Hypersensitive reaction of plant cytoplasm against incompatible inhibitor” is suggested. When such an incompatible inhibitor is introduced and brought in contact with cytoplasm, the latter lose its capability to adsorb virus particles as the results of disorganization due to its hypersensitivity.
In the cases of short feeding period of 15 to 20 seconds of M. persicae, the stylet is hardly capable to penetrate through the epidermal layer after it is inserted in between two epidermal cells, and the stylet borne virus as DMV is likely to be transmitted to the plasmodesmata in the intercellular region when stylet tip reaches there. In contrast to this, when DMV is inoculated by abrasion, cuticular layer of the leaf epidermis is scratched off, and the virus is transmitted easily to the disclosed ectodesmata. This histological difference of infectible sites in an epidermal cell-the one plasmodesmata for aphid inoculation, and the other ectodesmata for rubbing inoculations-is the decisive factor why Chenopodium sap is able to inhibit the infection of the virus only when the latter is inoculated by abrasion (Fig. 3).