RESUMEN
BACKGROUND: The presence of geminivirus sequences in a preliminary analysis of sRNA sequences from the leaves of macadamia trees with abnormal vertical growth (AVG) syndrome was investigated. RESULTS: A locus of endogenous geminiviral elements (EGE) in the macadamia genome was analysed, and the sequences revealed a high level of deletions and/or partial integrations, thus rendering the EGE transcriptionally inactive. The replication defective EGE in the macadamia genome indicates its inability to be the source of new viral infections and thus cause AVG or any other disease in macadamia. The EGE sequences were detected in two edible Macadamia species that constitute commercial cultivars and the wild germplasm of edible and inedible species of Macadamia. This strongly suggests that the integration preceded speciation of the genus Macadamia. A draft genome of a locus of EGE in Macadamia was developed. The findings of this study provide evidence to suggest the endogenization of the geminiviral sequences in the macadamia genome and the ancestral relationship of EGE with Macadamia in the Proteaceae family. Random mutations accumulating in the EGE inform that the sequence is evolving. CONCLUSIONS: The EGE in Macadamia is inactive and thus not a direct cause of any diseases or syndromes including AVG in macadamia. The insertion of the EGE in the macadamia genome preceded speciation of the genus Macadamia.
Asunto(s)
Genoma , Macadamia , Macadamia/genéticaRESUMEN
Australian macadamia production is threatened by a disorder known as abnormal vertical growth (AVG), for which the etiology is unknown. AVG is characterized by vigorous upright growth and reduced lateral branching, flowering, and nut set that results in over 70% yield loss annually. Six commercial macadamia orchards were surveyed in 2012 and again in 2018 to examine spatiotemporal dynamics of the epidemic. Data were subjected to point-pattern and geostatistical analyses. AVG incidence in all orchards showed a better fit to the beta-binomial distribution than the binomial distribution. AVG incidence in the different orchards varied between 5 and 47% in 2012, and 13 and 55% in 2018 and the rate of spread was slow, averaging at about 2% increase in disease incidence per annum. Spatial patterns of AVG were highly aggregated on both survey years and spread was mainly between neighboring trees in a row or trees that were opposite to each other in different rows. Semivariograms showed large range values (approximately 15 to 120), indicating aggregation of AVG-affected trees beyond quadrat levels. Furthermore, clusters of disease were mainly at the edge of the orchard on the first survey date and the disease progressed toward the center of the orchard over time. It is concluded that AVG is caused by an infectious agent, and based on patterns of spread, we hypothesize that spread is facilitated by root grafting or root-to-root contact. Furthermore, a vascular-limited pathogen could be involved that modulates plant hormone production.
