Arabidopsis mutants that suppress the phenotype induced by transgene-mediated expression of cauliflower mosaic virus (CaMV) gene VI are less susceptible to CaMV-infection and show reduced ethylene sensitivity.

Protein P6 is the main symptom determinant of cauliflower mosaic virus (CaMV), and transgene-mediated expression in Arabidopsis induces a symptom-like phenotype in the absence of infection. Seeds of a P6-transgenic line, A7, were mutagenized by gamma-irradiation and M2 seedlings were screened for mutants that suppressed the phenotype of chlorosis and stunting. We identified four mutants that were larger and less chlorotic than the A7 parent but which contained an intact and transcriptionally active transgene. The two mutants with the strongest suppression phenotype, were recessive and allelic. The transgene was eliminated by back-crossing with wild-type Arabidopsis. In progeny lines that were homozygous for the putative suppressor mutation the proportion of plants becoming infected following inoculation with CaMV was 40% that of wild-type, although in plants that did become infected, levels of virus DNA in mutants and wild-type did not differ significantly. Symptoms in the mutants were milder and delayed although this was somewhat dependent on the virus isolate. This phenotype was inherited stably. Both mutant alleles showed a partially ethylene-insensitive phenotype in an ethylene triple response assay. P6-transgenic plants were also almost completely insensitive to ethylene in the triple response assay. We suggest that the chlorosis and stunting in P6-transgenic and CaMV-infected plants are dependent on interactions between P6 and components involved in ethylene signalling, and that the suppressor gene product may function to augment these interactions.

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.