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Tobacco plants respond to the constitutive expression of the tospovirus movement protein NS M with a heat‐reversible sealing of plasmodesmata that impairs development
Author(s) -
Rinne Päivi L.H.,
Boogaard Riki van den,
Mensink Ma G.J.,
Kopperud Cor,
Kormelink Richard,
Goldbach Rob,
Schoot Chris van der
Publication year - 2005
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/j.1365-313x.2005.02489.x
Subject(s) - plasmodesma , callose , shoot , rosette (schizont appearance) , tobacco mosaic virus , biology , movement protein , botany , elongation , apoplast , nicotiana tabacum , tobamovirus , arabidopsis thaliana , chlorosis , haustorium , virus , cell wall , mutant , virology , biochemistry , coat protein , immunology , rna , materials science , ultimate tensile strength , gene , metallurgy , ecology , host (biology)
Summary Viral infection often results in typical symptoms, the biological background of which has remained elusive. We show that constitutive expression of the NS M viral movement protein (MP) of tomato spotted wilt virus in Nicotiana tabacum is sufficient to induce severe, infection‐like symptoms, including pronounced deficiencies in root and shoot development. Leaves failed to expand and were arranged in a rosette due to the absence of internode elongation. Following the sink–source transition they accumulated excessive amounts of starch and developed fusing chlorotic patches in the mesophyll, resembling virus‐induced chlorotic lesions. Eventually, the leaves became entirely white and brittle. With a combination of techniques, including photosystem II quantum‐yield measurements, iontophoresis of symplasmic tracers, bombardment with pPVX.GFP and double immunolabelling it was shown that these symptoms correlated with the obstruction of NS M ‐targeted mesophyll plasmodesmata (Pd) in source tissues by depositions of 1,3‐ β ‐D‐glucan (GLU) or callose. Temperature‐shift treatments (TST; 22→32°C), known to abolish chlorotic local lesions, also abolished the chlorotic ‘superlesions’ of transgenic plants and rescued plant development, by restoring the transport capacity of Pd through the action of 1,3‐ β ‐D‐glucanase (GLU‐h) or callase. Return of these elongated, TST‐recovered plants to 22°C reintroduced superlesions and arrested shoot elongation, resulting in the formation of a rosette of clustered leaves at the shoot tip. Collectively, this indicates that the symptoms of NS M plants are self‐inflicted and due to a basal defence response that counteracts prolonged interference of the MP with Pd functioning. This type of defence may also play a role in the formation of symptoms during viral infection.