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

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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. amaranticocor plants. Ten to thirty days after inoculation, several necrotic spots which have no connection with the primary 1oca1 1esions on the inoculated leaves were produced abruptly on upper youngl eaves. These necrotic spots were tentatively ca11ed "trans1ocated necrotic lesions" (TNLs, Fig. 1and 3). In the case of Chenopodium plants, daily production of TNLs gradua11y decreased in number, and sixty to hundred days after inoculation TNLs formation stopped completely. It was found that no TNL was produced on meristematic tissues of stem apices and also on mature leaves. 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 cha11enge inoculation of the same virus (Fig, 2). 2) Local 1esion 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 s1ightlyl be1ow the stem apex (Fig. 4 and Fig. 5). In the case of N. sylvestris plants, TNLs were frequently produced on midribs. Un1ike the case of Chenopodium plants, TNLs on young leaves near the stem apex of Nicotiana plants increased gradua11y inn umber and also enlarged themselves throughout the stem apex. The necrotic portions then extended downwards, and resulted fina11y in the death of the whole shoots of the necrotic hosts. Recovery of the inoculated virus from TNLs on Nicotiana plants was successful, whi1e from the leaf portion outside of TNLs it was unsuccessful. Moreover, no cross protection reaction of the non-necrotic portions of the leaf against cha11enge inocu1ation of the same virus was observed. 3) The mechanisms of TNL formation and the cause of the regularity of TNL distribution with in the shoot of necrotic host plants have been explained, according to the hypothesis of "transcription of viral code by the host ce11" reported elsewhere 43) as fo11ows: 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 ce11 having nucleus so far grown to be able to transcribe the viral code, the ce11 will reproduce the virus. When the code-carrying double stranded RNA is translocated in to a mature ce11 of the necrotic host, the carrier wi11 soon be degraded with in the cytoplasm. Thus regularity in distribution of the translocated necrotic lesions on the affected shoots ensues.
日本植物病理学会の論文
1969-06-30

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

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