A plant virus evolved by acquiring multiple nonconserved genes to extend its host range.

The Biological Evolution has always progressed from some simpler forms to some complex forms. It is a well established fact that the higher organism contains some genomic imprints  (i.e. genomic regions similar to that of the simpler organisms) of their ancestors which well proves the course of evolution. Even in human, more than 90% of their genome are non-functional chunks of DNA fragments which they share with their ancestors and other organisms. But sometimes, in the course of evolution, the simpler organism can interact with the complex/higher organism and have some functional advantage that helps the simpler organism to survive in the nature.

A recent paper published in PNAS indicates similar concept.

A plant virus evolved by acquiring multiple nonconserved genes to extend its host range.

Tatineni S, Robertson CJ, Garnsey SM, Dawson WO.
Citrus Research and Education Center, University of Florida- Institute of Food and Agricultural Sciences, Lake Alfred, FL 33850.
Viruses have evolved as combinations of genes whose products interact with cellular components to produce progeny virus throughout the plants. Some viral genes, particularly those that are involved in replication and assembly, tend to be relatively conserved, whereas other genes that have evolved for interactions with the specific host for movement and to counter host-defense systems tend to be less conserved. Closteroviridae encode 1-5 nonconserved ORFs. Citrus tristeza virus (CTV), a Closterovirus, possesses nonconserved p33, p18, and p13 genes that are expendable for systemic infection of the two laboratory hosts, Citrus macrophylla and Mexican lime. In this study, we show that the extended host range of CTV requires these nonconserved genes. The p33 gene was required to systemically infect sour orange and lemon trees, whereas either the p33 or the p18 gene was sufficient for systemic infection of grapefruit trees and the p33 or the p13 gene was sufficient for systemic infection of calamondin plants. Thus, these three genes are required for systemic infection of the full host range of CTV, but different genes were specific for different hosts. Remarkably, either of two genes was sufficient for infection of some citrus hybrids. These findings suggest that CTV acquired multiple nonconserved genes (p33, p18, and p13) and, as a result, gained the ability to interact with multiple hosts, thus extending its host range during the course of evolution. These results greatly extend the complexity of known virus-plant interactions.

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