Abstract

Pinto bean primary leaves infected with TMV-U1 produce small lesions. However, when leaves were irradiated with ultraviolet light (UV) 24 hours after inoculation, larger lesions developed in 1–2 days and subsequently enlarged when the leaves were kept dark (21–28 °). The mechanism of increasing lesion size by UV irradiation was investigated to clarify its effect on virus spread from cell to cell and the nature of resistance of the untreated leaf cells to viral movement. Unirradiated control leaves formed small necrotic lesions involving mostly the upper epidermis and palisade tissue and only a small proportion of spongy tissue. One to two days after the upper side of the leaf was irradiated, necrosis involved a larger area of the upper epidermis and palisade layers and subsequently slowly involved spongy tissue. However, when the lower side of the leaf was irradiated, lesions in cross section resembled an inverted funnel shape necrosis involving mainly the lower epidermis and spongy parenchyma. The results may be interpreted as a weakening of the cellular resistance mechanism in UV-irradiated and darkened leaves. Callose deposition induced by necrosis was correlated with the rate of movement of TMV from infected to noninfected cells. Callose deposition was prevented by UV irradiation and darkening. The shape of the necrotic lesions seems to be correlated with the facility of spread of TMV into different tissues. When virus moved vertically from the inoculated upper epidermis to the lower epidermis through palisade and spongy tissues, UV irradiation of the lower side was not sufficiently strong to prevent callose deposition on the upper epidermal cells. Lateral movement of virus was mainly through the lower spongy layer and lower epidermis, producing a lesion shaped like an inverted funnel. In nonirradiated lesions, palisade parenchyma became necrotic only in cells directly under the necrotic upper epidermal cells, which were surrounded by a callose band. Apparently, there was no lateral movement of TMV in palisade parenchyma even though there was no conspicuous callose deposition on the walls of surrounding palisade parenchyma adjacent. This may be attributed to the paucity of lateral contact among palisade parenchyma cells. There was heavy deposition of callose in the spongy parenchyma adjacent to necrotic palisade or spongy cells, accounting for the usual lack of spread of necrosis into the lower spongy layer. When the upper side of the leaves was irradiated, no callose band was formed, and necrosis occurred in the upper epidermis and palisade cells. Lesions enlarged with time, but spongy cells were less involved. The UV doses used apparently did not reach the spongy tissue with sufficient intensity to prevent callose deposition there.

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