SummaryViral 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-b-D-glucan (GLU) or callose. Temperature-shift treatments (TST; 22 fi 32°C 1 ), 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-b-D-glucanase (GLU-h) or callase. Return of these elongated, TSTrecovered 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.