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The biology and epidemiology of Stylosanthes little leaf disease

De La Rue, Stephanie J. (2003). The biology and epidemiology of Stylosanthes little leaf disease. PhD Thesis, Northern Territory University.

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Author De La Rue, Stephanie J.
Title The biology and epidemiology of Stylosanthes little leaf disease
Institution Northern Territory University
Publication Date 2003
Thesis Type PhD
Subjects 0607 - Plant Biology
Abstract This research was undertaken to determine the effect of phytoplasma associated diseases on Stylosanthes spp. and clarify the relationship between the "little leaf' and "reversion" disease syndromes. Preliminary surveys of Stylosanthes stands in Queensland (Qld) and the Northern Territory (NT) identified the phytoplasmas pigeon pea little leaf (PLL), sweet potato little leaf variant V4 (SPLL-V4) and stylosanthes little leaf (StLL) in association with a wide range of symptoms such as leaf size reduction, side shoot proliferation and floral deformation. In addition to these three pathogens, the phytoplasma vigna little leaf (ViLL) was also detected in one sample from the NT but was never identified in samples from Qld. Genetic studies of the ribosomal operons of these phytoplasmas found that StLL was unique, having ribosomal operons both with and without the characteristic tRNAlle gene within the 16S-23S intergenic spacer region. The combination and severity of symptoms expressed by plants with stylosanthes little leaf disease was highly variable making it difficult to correlate symptom type with phytoplasma strain. As a result no pathogen specific disease description could be made. Instead the term stylosanthes little leaf (SLL) disease was adopted to refer to all phytoplasma associated diseases of this host. The most accurate indicator of SLL disease was found to be reduction in leaf size (little leaf) which usually occurred in association with side shoot proliferation. Further studies of the floral symptoms expressed by diseased plants showed that particular types of floral deformation could be associated (p = 0.1) with specific phytoplasma strains. Namely, phyllody was associated with PLL, while virescence was often associated with SPLL-V4. This finding was not used to formulate a pathogen specific symptom description because of the seasonal nature of this symptom and the small size of stylo flowers which makes the accurate identification of different types of floral deformation problematic. To determine the susceptibility of members of the genus Stylosanthes to SLL disease 23 varieties were surveyed for phytoplasma associated symptoms over the 1999 growing season. Included in this trial was Stylosanthes scabra cvv Seca, Siran, and Fitzroy, S. guianensis var. guianensis cv Cook, S. hamata cvv Amiga and Verano and "Stylosanthes seabrana" cvv Unica and Primar, as well as seven unreleased cultivars from a CSIRO anthracnose resistance breeding program, and four unreleased introduced lines. Except S. hamata cv. Verano and "Stylosanthes seabrana" cv. Unica, all taxa were found to be susceptible to SLL disease, although the S. scabra varieties were found to have the highest disease incidence, with many varieties having significantly higher levels of disease than that of the original introductions from which they were derived. To study the spatial and temporal dynamics of SLL disease 2500 S. scabra cv. Seca plants were studied over two seasons (1999 & 2000). The incidence of SLL disease differed considerably between seasons, with a total of 15.4% of plants in 1999 being found positive for the SLL phytoplasmas (PLL, SPLL-V4 and StLL), while 40.4% were phytoplasma positive in 2000. The impact of these pathogens on the longevity of infected plants was minimal, with only 1.1% and 4.3% of diseased plants dying in the 1999 and 2000 seasons, respectively. Of the diseased plants that did die, those affected by mixed infections of StLL with either PLL or SPLL-V4 were more likely to die than those affected by any of the phytoplasma strains on their own. Comparisons of the increase in each phytoplasma strain over the two seasons indicated that the 1999 and 2000 epidemics progressed quite differently. In both years spatial analysis was used to identify clusters of diseased plants within the trial. Spatiotemporal analysis of these clusters indicated that they did not expand over time, suggesting that spread of disease from one diseased plant to adjacent plants was uncommon which is consistent with the transmission of SLL disease by a mobile aerial vector. To determine the effect of SLL disease and the time of infection on seed yield, both diseased and asymptomatic Seca plants were harvested at the end of the 1999 and 2000 seasons. Plants that first showed symptoms after flowering for less than 30 days did not produce significant amounts of seed. Yield continued to be low until plants had flowered for at least 60 days before symptom expression, after which yield was extremely variable but within the range of that observed for individual asymptomatic plants. The small number of fatalities due to SLL and the minimal effect this disease has on seed yield means that, except in unusual circumstances, SLL is unlikely to adversely effect the productivity of commercial seed crops in north Queensland.


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