Mutants of African cassava mosaic virus containing extensive deletions across the coat protein gene that remove up to one-third of the genomic component have been constructed and shown to be infectious when mechanically inoculated onto by leaf abrasion. Using protoplasts we demonstrate that mutant pCLV. CPΔ11, containing a 712 bp deletion, is competent for replication in its deleted form. However, systemic spread of pCLV. CPΔ11 and other deletion mutants is associated with reversion of DNA 1 to a size comparable to that of the native genomic component. This contrasts with the behaviour of coat protein mutants of the closely related geminivirus tomato golden mosaic virus which maintain their deletions during spread. Appraisal of the different inoculation procedures used to introduce the mutants into plants suggests the imposition of a stringent size requirement for localized cell-to-cell spread which is relaxed for long distance spread through the vascular system.

Keyword(s): ACMV , coat protein and geminivirus

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