Invasive plants cost Australia, directly and indirectly, around AU$4 billion pa; displacing native species, changing sensitive ecosystems and sometimes affecting human health and safety. Developing novel tools to control invasive species will benefit landholders and the environment, not just in Australia, but globally. Biocontrol of invasive plants via dieback causative agents is one such potential tool. Dieback causes a progressive reduction in plant population health, resulting in the death of plant parts and often complete plant death. It is prevalent in many invasive woody weeds in Australia and has been suggested as a potential mechanism for their biocontrol, particularly because local native plants appear unaffected.
Parkinsonia aculeata L. (Fabaceae; referred to hereafter as “parkinsonia”) is an invasive tree in northern Australia, with native populations in South and Central America and southern USA. It is a perennial thorny shrub that forms dense thickets along waterways, floodplains and throughout paddocks, seriously impacting the pastoral industry, local biodiversity, and providing shelter to other invasive species such as feral pigs. Some Australian parkinsonia populations are affected by dieback, resulting in localised control. Despite previous and ongoing research, the cause of parkinsonia dieback remains elusive and dieback has not been observed in parkinsonia’s native range. This thesis investigates the potential cause(s) of dieback in parkinsonia to contribute towards research on determining its suitability as a biological control tool. My goals were to describe the microbial endophytes of parkinsonia, identify correlations of microbial community composition and dieback occurrence, and identify patterns and pathogens that might be involved in dieback. First, I analysed the community composition of archaeal, bacterial and fungal endophytes from the roots, stems and stem tips of healthy and dieback-affected parkinsonia. Samples were taken from Charters Towers in Queensland (QLD), Australia in May 2013. I used terminal restriction fragment length polymorphism (T-RFLP) analysis with taxon-specific primers for archaea, bacteria and fungi, followed by statistical analysis to determine how endophyte community composition relates to plant part and disease status. Archaeal and fungal community structures were significantly correlated with dieback occurrence and plant part. Bacterial community composition showed significant correlation to dieback occurrence but not plant part. The results showed that endophyte community composition in parkinsonia is associated with the occurrence of dieback and that endophyte communities vary across plants parts. I hypothesised that dieback occurrence may be due to the lack of potentially protective endophytes or the presence of putative pathogens. As a complimentary study to the T-RFLP analysis, I used the same samples collected in QLD to characterise the culturable fungal endophyte communities in healthy and dieback-affected parkinsonia. I identified 219 isolates via amplicon sequencing of the internal transcribed spacer (ITS) to reveal a library of 54 unique species from 25 families. Eight isolates, identified as putative pathogens, were selected for a 10-week pathogenicity trial, including water stress treatments, on parkinsonia seedlings to determine whether inoculations of parkinsonia with these isolates would result in dieback-like symptoms, and whether stress due to drought or inundation enhanced these responses. Of the eight putative pathogenic isolates tested in the pathogenicity trial, inoculation with Lasiodiplodia pseudotheobromae, Botryosphaeria dothidea and Pestalotiopsis mangiferae resulted in the largest lesions, but systemic infection or dieback-like symptoms were not observed, despite significant reductions in plant health due to water stress. As systemic infection or dieback symptoms were not observed, I determined that these pathogens are either not involved in parkinsonia dieback, that different or more extreme abiotic or biotic stress levels are required to trigger dieback-like symptoms, or that changes to the inoculation method are needed. Combining these factors will be essential in evaluating which factors are most important in initiating dieback in parkinsonia.
Determining the cause of dieback in affected weeds may present land managers with a ‘silver bullet’ of biological control that could become a self-managed, perpetual instrument, reducing weed management costs and increasing biodiversity and land productivity. As such, future work in the use of dieback and host-specific phytopathogens for biological control of invasive plants should continue
