ウイルス病に感染した局部壊死斑寄主における壊死斑の転移

1) Daikon mosaic virus (DMV: the Japanese strain of turnip mosaic virus) and tobacco mosaic virus (TMV) were sap inoculated on leaves of Chenopodium album or of C. amaranticolor plants. Ten to thirty days after inoculation, several necrotic spots which have no connection with the primary local lesions on the inoculated leaves were produced abruptly on upper young leaves. These necrotic spots were tentatively called “translocated necrotic Lesions” (TNLs, Fig. 1 and 3). In the case of Chenopodium plants, daily production of TNLs gradually decreased in number, and sixty to hundred days after inoculation TNL formation stopped completely.<br>It was found that no TNL was produced on meristematic tissues of stem apices and also on mature leaves.<br>From TNLs the viruses were recovered easily, while attempts to recover the viruses from non-necrotic portions of the same leaves were unsuccessful. Moreover, the leaf with TNLs showed no cross protection reaction against challenge inoculation of the same virus (Fig. 2).<br>2) Local lesion hosts of tobacco mosaic virus-tomato strain (TMV-T), Nicotiana sylvestris or N. glutinosa plants were grafted with N. tabacum var. Xanthi, a systemic (mosaic) host of the virus strain. One to two months after grafting, the virus was inoculated on leaves of the Xanthi part of the grafted plant. Forty to sixty days after inoculation of the virus, TNLs were produced abruptly on young leaves of the necrotic lesion hosts slightly below the stem apex (Fig. 4 and Fig. 5). In the case of N. sylvestris plants, TNLs were frequently produced on midribs.<br>Unlike the case of Chenopodium plants, TNLs on young leaves near the stem apex of Nicotiana plants increased gradually in number and also enlarged themselves throughout the stem apex. The necrotic portions then extended downwards, and resulted finally in the death of the whole shoots of the necrotic hosts.<br>Recovery of the inoculated virus from TNLs on Nicotiana plants was successful, while from the leaf portion outside of TNLs it was unsuccessful. Moreover, no cross protection reaction of the non-necrotic portions of the leaf against challenge inoculation of the same virus was observed.<br>3) The mechanisms of TNL formation and the cause of the regularity of TNL distribution within the shoot of necrotic host plants have been explained, according to the hypothesis of “transcription of viral code by the host cell” reported elsewhere⁴³⁾ as follows:<br>The viral code carried by double stranded TMV-RNA is translocated from the primary necrotic lesions to the growing tissues of young shoots via sieve tube. When the code is transferred to a young cell having nucleus so far grown to be able to transcribe the viral code, the cell will reproduce the virus. When the code-carrying double stranded RNA is translocated into a mature cell of the necrotic host, the carrier will soon be degraded within the cytoplasm. Thus regularity in distribution of the translocated necrotic lesions on the affected shoots ensues.