Abstract
A deletion mutant of cauliflower mosaic virus (CaMV) isolate NY8153 deficient in aphid transmissibility was constructed by BAL-31 exonuclease treatment of XhoI linearized pCMS31 (a plasmid containing the entire CaMV genome cloned in the SalI site of pBR322), followed by ligation. The resulting mutant, pSA103, lacked about 100 by from the putative protein-coding region II of CaMV DNA. In turnips there was no difference in the number and appearance of starch lesions or hybridization lesions, or in the nature of symptoms in systemically infected leaves induced by pSA103 DNA, pCMS31 DNA, and NY8153 DNA. Systemic symptoms appeared later in plants infected with pSA103 (27 ± 2 days) than in those infected with the parental pCMS31 DNA (19 ± 2 days). Aphids fed on virus SA103-infected mustard plants were unable to transmit the virus to healthy plants while 30–70% transmission was observed from plants infected by the parent virus. Virions extracted from turnips infected with the mutant had DNA still containing the deletion. In addition, the single-stranded discontinuity in region II of NY8153 DNA was missing in this DNA. The results suggest that region II codes for a “helper component” required for aphid transmission of CaMV.
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