Abstract

Ageratum yellow vein disease (AYVD) is caused by the geminivirus ageratum yellow vein virus (AYVV) and an associated DNA β satellite. We have mapped a DNA β transcript to a highly conserved open reading frame (βC1 ORF). The most abundant transcript 5′-terminus is located 8 bases upstream of the βC1 ORF putative initiation codon while the transcript terminates at multiple sites downstream from the putative termination codon. Disruption of βC1 protein expression by the introduction of an internal nonsense codon prevented infection of the AYVV–satellite complex in ageratum and altered the phenotype in Nicotiana benthamiana to that produced by AYVV alone although the mutant was maintained in systemically infected tissues. Modification of the putative initiation codon to a nonsense codon produced an intermediate phenotype in N. benthamiana and a mild yellow vein phenotype in ageratum, suggesting that βC1 protein expression could be initiated from an alternative site. N. benthamiana plants containing a dimeric DNA β transgene produced severe developmental abnormalities, vein-greening, and cell proliferation in the vascular bundles. Expression of βC1 protein from a potato virus X (PVX) vector also induced abnormal plant growth. Our results demonstrate that the satellite encodes at least one protein that plays a major role in symptom development and is essential for disease progression in ageratum, the natural host of the AYVD complex.

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