Investigating eucalypt diseases of unknown etiology: The Mundulla Yellows experience

Also cited as: Proceedings of the IInd international symposium on guava and other Myrtaceae : Mérida, Mexico November 10-13, 2008; Aguascalientes, Mexico November 17-18, 2008 / W. Rohde and G. Fermin (eds.): pp. 325-330

Diseases of eucalypts cause significant losses worldwide. Pathogens include Phytophthora spp., fungi, bacteria and phytoplasmas, but so far no viruses have been isolated or characterised from eucalypts despite observations of mosaic, chlorosis, leaf curl and leaf spot symptoms. A new lethal dieback disease of Australian eucalypts, known as Mundulla Yellows (MY) has emerged as a threat to natural vegetation, ancient iconic trees, natural wildlife habitats and conservation programs. Symptoms are an asymmetric progressive yellowing and slow dieback of the crown. Similar symptoms have been observed in eucalypts growing in Spain, Peru and Syria. No fungi, bacteria or phytoplasmas were found to be associated with MY. Traditional infectivity assays were unsuitable for testing whether MY is a virus-associated disease, so component analysis is being used to seek disease-associated nucleic acids or proteins which may implicate a virus-like agent in the etiology of MY. A number of physically distinct small RNAs were found preferentially in diseased trees, but none had sequences related to those of known viruses. Specific nucleoprotein fractions from MY affected trees contained disease-associated 84 kDa and 116 kDa proteins and quasi-spherical particles 30-40 nm in diameter. Limited sequence analysis of the 84 kDa protein and RNA also associated with the nucleoprotein fraction showed that neither had similarities to known plant viruses. It is concluded that the diseaseassociated nucleic acids and proteins could either be components of a previously undescribed type of intracellular plant pathogen, or host products resulting from pathogenic changes in affected trees. Targets for future research are the 30-40 nm particles, and the MY associated protein.

J. W. Randles, D. Hanold, M. Stukely and N. Thompson

http://www.actahort.org/books/849/849_38.htm