Some strains of Pseudomonas syringae pv. actinidiae (Psa), the causal agent of bacterial canker of kiwifruit, produce plant hormones and toxins which alter the plant hormonal balance and result in the suppression of the salicylic acid (SA)-dependent plant defences. To determine whether Psa could be affected by stimulation of the SA pathway, Actinidia deliciosa and A. chinensis were treated with compounds which interfere with this pathway, then inoculated with Psa. On A. deliciosa, compounds which stimulate the SA pathway [SA, or its synthetic analogue, acibenzolar-S-methyl (ASM)] or close stomata (ABA) resulted in disease reduction, while methyl-jasmonate (MJA) or ethylene increased disease development. On A. chinensis, similar results were obtained except that SA and MJA did not affect disease development. Reduction in disease incidence and severity on A. deliciosa using ASM was correlated with a superoxide burst, the formation of necrotic spots and callose deposition, while on A. chinensis no superoxide burst or callose deposition was detected. Genes involved in plant-pathogen interactions were induced after treatment with ASM in A. deliciosa and, to a lesser extent, in A. chinensis. Those differences in gene expression and physiological responses after treatment with ASM are consistent with the different susceptibility to Psa observed between A. chinensis and A. deliciosa.
Since 2008, the kiwifruit industry has been devastated by a pandemic outbreak of Pseudomonas syringae pv. actinidiae (Psa), the causal agent of bacterial canker. This disease has become the most significant limiting factor in kiwifruit production. Psa colonizes different organs of the host plant, causing a specific symptomatology on each of them. In addition, the systemic invasion of the plant may quickly lead to plant death. Despite the massive risk that this disease poses to the kiwifruit industry, studies focusing on Psa ecology have been sporadic, and a comprehensive description of the disease epidemiology is still missing. Optimal environmental conditions for infection, dispersal and survival in the environment, or the mechanisms of penetration and colonization of host tissues have not been fully elucidated yet. The present work aims to provide a synthesis of the current knowledge, and a deeper understanding of the epidemiology of kiwifruit bacterial canker based on new experimental data. The pathogen may survive in the environment or overwinter in dormant tissues and be dispersed by wind or rain. Psa was observed in association with several plant structures (stomata, trichomes, lenticels) and wounds, which could represent entry points for apoplast infection. Environmental conditions also affect the bacterial colonization, with lower optimum values of temperature and humidity for epiphytic than for endophytic growth, and disease incidence requiring a combination of mild temperature and leaf wetness. By providing information on Psa ecology, these data sets may contribute to plan efficient control strategies for kiwifruit bacterial canker. Keywords Actinidia chinensis Planch. var. chinensis. Actinidia chinensis var. deliciosa (A.Chev.). Temperature. Relative humidity. Confocal laser scanning microscopy (CLSM). Overwintering
In the current scenario of rapidly evolving climate change, crop plants are more frequently subjected to stresses of both abiotic and biotic origin, including exposure to unpredictable and extreme climatic events, changes in plant physiology, growing season and phytosanitary hazard, and increased losses up to 30% and 50% in global agricultural productions. Plants coevolved with microbial symbionts, which are involved in major functions both at the ecosystem and plant level. The use of microbial biostimulants, by exploiting this symbiotic interaction, represents a sustainable strategy to increase plant performances and productivity, even under stresses due to climate changes. Microbial biostimulants include beneficial fungi, yeasts and eubacteria sharing the ability to improve plant nutrition, growth, productivity and stress tolerance. This work reports the current knowledge on microbial biostimulants and provides a critical review on their possible use to mitigate the biotic and abiotic stresses caused by climate changes. Currently, available products often provide a general amelioration of cultural conditions, but their action mechanisms are largely undetermined and their effects often unreliable. Future research may lead to more specifically targeted products, based on the characterization of plant-microbe and microbial community interactions.
Abstract. Since 2008, Pseudomonas syringae pv. actinidiae, the causal agent of bacterial canker of kiwifruit has become the main pathogen of yellow and green fleshed kiwifruit. All major kiwifruit producing countries in the world have been affected by this bacterial pathogen, leading to substantial economic losses. This review presents the current knowledge on various aspects about the origin, epidemiology, detection and control strategies of Pseudomonas syringae pv. actinidiae.
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.
The use of lactic acid bacteria (LAB) to control multiple pathogens that affect different crops was studied, namely, Pseudomonas syringae pv. actinidiae in kiwifruit, Xanthomonas arboricola pv. pruni in Prunus and Xanthomonas fragariae in strawberry. A screening procedure based on in vitro and in planta assays of the three bacterial pathogens was successful in selecting potential LAB strains as biological control agents. The antagonistic activity of 55 strains was first tested in vitro and the strains Lactobacillus plantarum CC100, PM411 and TC92, and Leuconostoc mesenteroides CM160 and CM209 were selected because of their broad‐spectrum activity. The biocontrol efficacy of the selected strains was assessed using a multiple‐pathosystem approach in greenhouse conditions. L. plantarum PM411 and TC92 prevented all three pathogens from infecting their corresponding plant hosts. In addition, the biocontrol performance of PM411 and TC92 was comparable to the reference products (Bacillus amyloliquefaciens D747, Bacillus subtilis QST713, chitosan, acibenzolar‐S‐methyl, copper and kasugamycin) in semi‐field and field experiments. The in vitro inhibitory mechanism of PM411 and TC92 is based, at least in part, on a pH lowering effect and the production of lactic acid. Moreover, both strains showed similar survival rates on leaf surfaces. PM411 and TC92 can easily be distinguished because of their different multilocus sequence typing and random amplified polymorphic DNA profiles.
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