Systemic Infection of Tomato Bushy Stunt Virus in <i>Gomphrena globosa</i> Induced by High Temperature and Long Photoperiod

Redolfi, P.; Pennazio, S.; Appiano, Anna; Martı́n, Carmen

doi:10.1111/j.1439-0434.1977.tb02884.x

Cited by 8 publications

(2 citation statements)

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“…In Gomphrena globosa infected with tomato bushy stunt virus (TBSV) the change from hypersensitive local to systemic mottle infection is conditioned by both temperature and photoperiod (Redolfi et aL 1977). The course of the systemic infection is different from induced systemic infections hitherto described for other virus-host systems (Martin & Gallet, 1966;Carroll & Kosuge, 1969;Shimomura, 1971 ;Takahashi, 1975) in two respects: some localization remains and systemic infection is not blocked by restoring the environmental conditions which induce hypersensitivity.…”

Section: Introductionmentioning

confidence: 92%

“…We have suggested (Redolfi et al 1977) that in systemic infection the localizing mechanism preventing cell-to-cell spread of TBSV was not entirely suppressed. The present results confirm this: the necrotic lesions found in systemically invaded leaves, like those of the hypersensitive tissues, are surrounded by tissues lacking infectivity, virus particles and any pathological cytology.…”

Section: Green Regionsmentioning

confidence: 99%

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Cytological Alterations in Tissues of Gomphrena globosa Plants Systemically Infected with Tomato Bushy Stunt Virus

Appiano¹,

Pennazio²,

Redolfi³

1978

Journal of General Virology

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SUMMARYSpecial environmental conditions were used to induce systemic infection by tomato bushy stunt virus (TBSV) in Gomphrena globosa. Severe mottle symptoms were followed by the formation of necrotic lesions. The mottled tissue consisted of small patches of necrotic, chlorotic and green tissue closely intermingled. The ultrastructure of such systemically infected G. globosa leaves was investigated. In the mesophyll and bundle sheath cells of the chlorotic patches the chloroplasts were severely altered and often connected to multivesicular (MV) bodies, whose vesicles and vacuoles contained fibrillar material. The MV bodies are thought to originate from chloroplasts and may be involved in TBSV replication. Virus appeared in the cytoplasm and central vacuole as scattered particles or small paracrystalline aggregates. Dark spots, probably proteinaceous material, were present in the cytoplasm. The cells of the necrotic patches appeared completely collapsed and contained virus particles. The necrotic lesions were cytologically quite similar to those produced in hypersensitive conditions.

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Section: Introductionmentioning

confidence: 92%

Section: Green Regionsmentioning

confidence: 99%