Abstract
Flowers can provide a protected and nutrient-rich environment to the epiphytic microflora, thus representing a sensible entry point for pathogens such as Pseudomonas syringae pv. actinidiae (Psa). This bacterium can colonize both male and female Actinidia flowers, causing flower browning and fall, and systemic invasion of the host plant, eventually leading to its death. However, the process of flower colonization and penetration into the host tissues has not yet been fully elucidated. In addition, the presence of Psa in the pollen from infected flowers, and the role of pollination in the spread of Psa requires confirmation.The present study employed a Psa strain constitutively expressing the fluorescent GFPuv protein, to visualize in vivo flower colonization. Microscopy observations were performed by means of confocal laser scanning and wide-field fluorescent microscopy, and were coupled with the study of Psa population dynamics by quantitative PCR (q-PCR). The pathogen was shown to colonize stigmata, move along the stylar furrow, and penetrate the receptacles via the style or nectarhodes. Once the receptacle was invaded, the pathogen migrated along the flower pedicel and became systemic. Psa was also able to colonize the anthers epiphytically and endophytically. Infected male flowers produced contaminated pollen, which could transmit Psa to healthy plants. Finally, pollinators (Apis mellifera and Bombus terrestris) were studied in natural conditions, showing that, although they can be contaminated with Psa, the pathogen’s transmission via pollinators is contrasted by its short survival in the hive.
Highlights
Among the production constraints of kiwifruit, the bacterial canker, caused by Pseudomonas syringae pv. actinidiae (Psa), has been the major limiting factor in the main growing areas worldwide since its pandemic outbreak in 20081–3
Biological material Experiments in controlled conditions were performed on kiwifruit cultivars Hayward, Tomuri, Hort16A and CK2, using 4-year-old potted plants maintained in plastic pots (40 cm diameter) with a mixture of peat and sand (1:1, v/v)
Psa was able to establish a detectable population on all the flowers parts of both A. chinensis var. chinensis and A. chinensis var. deliciosa female flowers (Fig. 1a, b)
Summary
Among the production constraints of kiwifruit, the bacterial canker, caused by Pseudomonas syringae pv. actinidiae (Psa), has been the major limiting factor in the main growing areas worldwide since its pandemic outbreak in 20081–3. Among the production constraints of kiwifruit, the bacterial canker, caused by Pseudomonas syringae pv. Actinidiae (Psa), has been the major limiting factor in the main growing areas worldwide since its pandemic outbreak in 20081–3. The disease affects various species of the genus Actinidia, including the two most important varieties for commercial purposes, A. chinensis var. In Italy, the first outbreak of bacterial canker was reported in 19947, but serious economic damage started being observed with the spread of a highly virulent pathogen, named biovar 3, genetically separated from previously identified biovars[8,9,10,11,12]. A few short communications have listed plant organs in which the pathogen was detected[13,14]. The detection of an endophytic pathogen within a specific
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