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Viruses induce pathogenic symptoms on plants but the molecular basis is poorly understood. Here, we show that transgenic  Arabidopsis  expressing the pathogenesis protein βC1 of  Tomato yellow leaf curl China virus  (TYLCCNV), a geminivirus, can phenocopy to a large extent disease symptoms of virus-infected tobacco plants in having upward curled leaves, radialized leaves with outgrowth tissues from abaxial surfaces, and sterile flowers. These morphological changes are paralleled by a reduction in miR165/166 levels and an increase in  PHB  and  PHV  transcript levels. Two factors, ASYMMETRIC LEAVES 1 (AS1) and ASYMMETRIC LEAVES 2 (AS2), are known to regulate leaf development as AS1/AS2 complex. Strikingly, βC1 plants phenocopy plants overexpressing AS2 at the morphological and molecular level and βC1 is able to partially complement  as2  mutation. βC1 binds directly to AS1, elicits morphological and gene expression changes dependent on AS1 but not AS2, and attenuates expression of selective jasmonic acid (JA)-responsive gene. Our results show that βC1 forms a complex with AS1 to execute its pathogenic functions and to suppress a subset of JA responses.

βC1, the pathogenicity factor of TYLCCNV, interacts with AS1 to alter leaf development and suppress selective jasmonic acid responses