Mutations that delay flowering in Arabidopsis de-couple symptom response from cauliflower mosaic virus accumulation during infection.

summary The development of disease symptoms in plants infected with a compatible virus involves complex signalling interactions between host and viral gene products. Photoperiod is an important influence on the transition from vegetative growth to flowering. Symptoms in wild-type Arabidopsis plants grown under long days were much less severe than in plants grown under short days, although under long days, the levels of replicating virus were 1.5-1.8 times greater than in plants grown in short days. We tested the effects on response to CaMV infection of mutations at two of the loci that control the transition from vegetative growth to flowering, FCA and GI. In long days, CaMV-infected fca-1 mutants and strong gi alleles developed much more severe symptoms than wild-type. Despite the increased symptom severity, levels and distribution of replicating CaMV in fca-1 and gi mutants were similar to those in wild-type. In short days, both mutants and wild-type grew vegetatively. Virus accumulation and symptom developments in fca-1 were similar to the wild-type, but in strong gi alleles, symptom progression in apical leaves was very delayed, although virus accumulation was similar to the wild-type controls. The developmental state of the plants influences the symptom response; however, it does not appear to do so by directly effecting overall virus titre or distribution. The altered symptom response of gi mutants in short days suggests an additional role for GI. These mutants provide compelling evidence for the existence of specific pathways for disease signalling.