Tobacco plants respond to the constitutive expression of the tospovirus movement protein NS(M) with a heat-reversible sealing of plasmodesmata that impairs development.

Viral infection often results in typical symptoms, the biological background of which has remained elusive. We show that constitutive expression of the NSM 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 NSM-targeted mesophyll plasmodesmata (Pd) in source tissues by depositions of 1,3-beta-D-glucan (GLU) or callose. Temperature-shift treatments (TST; 22-->32 degrees 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-beta-D-glucanase (GLU-h) or callase. Return of these elongated, TST-recovered plants to 22 degrees 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 NSM 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.