Screening of Antibacterial Lichen Extract and Streptomyces against Kiwifruit Bacterial Canker Pathogen, Pseudomonas syringae pv. actinidiae

2021 ◽  
Vol 25 (3) ◽  
pp. 221-229
Author(s):  
Su In Lee ◽  
Da-Ran Kim ◽  
Youn-Sig Kwak
1999 ◽  
Vol 154 (4) ◽  
pp. 489-497
Author(s):  
Maryke Appel ◽  
Mathias Hampf ◽  
Lucienne Mansvelt ◽  
Janet Hapgood ◽  
Dirk Bellstedt

2020 ◽  
Author(s):  
Takashi Fujikawa ◽  
Hiroe Hatomi ◽  
Hiroyuki Sawada

AbstractSeveral groups (biovars) of the kiwifruit bacterial canker pathogen, Pseudomonas syringae pv. actinidiae, are found in Japan. Here, we sequenced and compared the 10 genomes of biovar 1, the major group in Japan, which is known as the phaseolotoxin producer.The kiwifruit bacterial canker pathogen, Pseudomonas syringae pv. actinidiae (Psa), was first described in Japan in 1989 (1). Subsequently, Psa was found in other kiwifruit-producing countries (2). Based on comparative analyses (2–4), Psa was categorized into several groups (biovars). The first Japanese group was named biovar 1 (Psa1), which was also later found in Italy and Korea. This biovar produces phaseolotoxin (2), a phytotoxin that inhibits arginine biosynthesis in host plants and results in bacterial canker symptom development. On the Psa1 chromosome, a large number of genes involved in phaseolotoxin biosynthesis are accumulated in an approximately 23 kb region (argK-tox cluster), which is contained in an exogenous genomic island (tox island) that Psa1 acquired in the past (2). However, some Psa1 strains found in Ehime Prefecture, Japan (the Ehime isolates) do not produce phaseolotoxin, although they seem to possess the argK-tox cluster (5). On the other hand, several Psa1 strains preserved in the NARO Genebank (https://www.gene.affrc.go.jp/index_en.php) may lack this cluster (2). Here, we selected 10 strains (Table 1) that represent Psa1 diversity and conducted comparative genome analyses.


2020 ◽  
Author(s):  
Takashi Fujikawa ◽  
Hiroyuki Sawada

AbstractPseudomonas syringae pv. actinidiae is the pathogen that causes kiwifruit bacterial canker and is categorized into several groups (biovars). In Japan, biovar 3, known as the pandemic group, was first discovered in 2014. Here, we sequenced the genomes of nine Japanese biovar 3 strains.


2020 ◽  
Vol 9 (35) ◽  
Author(s):  
Takashi Fujikawa ◽  
Hiroe Hatomi ◽  
Hiroyuki Sawada

ABSTRACT Several groups (biovars) of the kiwifruit bacterial canker pathogen Pseudomonas syringae pv. actinidiae are found in Japan. Here, we sequenced and compared 10 genome sequences of biovar 1, a major group in Japan, which is known as the phaseolotoxin producer.


2020 ◽  
Vol 9 (45) ◽  
Author(s):  
Takashi Fujikawa ◽  
Hiroyuki Sawada

ABSTRACT Pseudomonas syringae pv. actinidiae is the pathogen that causes kiwifruit bacterial canker and is categorized into several groups (biovars). In Japan, biovar 3, known as the pandemic group, was first discovered in 2014. Here, we sequenced the genomes of nine Japanese biovar 3 strains.


2017 ◽  
Vol 70 ◽  
pp. 310-314
Author(s):  
J.L. Tyson ◽  
S.J. Dobson ◽  
M.A. Manning

Pseudomonas syringae pv. actinidiae (Psa) causes bacterial canker of kiwifruit, which is an ongoing threat to New Zealand kiwifruit production. Disease control depends on orchard practices such as removal of visibly diseased material, pruning during low-risk periods, and the application of foliar bactericides. Although the use of copper compounds on Actinidia species (kiwifruit) can cause phytotoxicity, copper-based formulations remain a key component of Psa control in New Zealand. The effect of single copper applications on Psa infection of ‘Hort16A’ trap plants was studied over the Spring of 2014 (Sept—Nov). Psa leaf spots were observed at the beginning of October, appearing first on the untreated plants. Although the copper sprays did not achieve complete protection, particularly as the inoculum built up during November, the copper-sprayed plants always had less disease than the untreated plants.


HortScience ◽  
1990 ◽  
Vol 25 (11) ◽  
pp. 1354F-1355
Author(s):  
Elzbieta Krzesinska ◽  
Anita Nina Miller

An excised twig assay was developed to evaluate cherry geno-types for their tolerance to Pseudomonas syringae pv. syringae. One-year-old wood was collected at monthly intervals from October until January of `Royal Ann', `Corum', and a number of cherry rootstock. The rootstock included; F/12–1 and Giessen (GI) and M × M selections. A 2-cm incision (“^”-shaped flap) was made on each twig. A 20-μl droplet of inoculum or water was placed onto each incision. The inoculum was prepared with one avirulent (K4) and three virulent strains (W4N54, AP2, B15) concentrations (105, 106, or 107 cfu). Inoculated twigs were placed in test tubes and incubated at 15C in high relative humidity for 3 weeks. After incubation, twigs were evaluated for gummosis production (0–3, 0 = no gummosis), incision browning (1–4, 1 = yellow pith), and callus production (0–1, 0 = no callus). The concentration of bacterial suspension had no effect on symptom development. No gummosis or browning was observed on twigs inoculated with water or the avirulent strain. Based on the gummosis and browning ratings, rootstock M × M 2, M × M 39, M × M 60, GI 148-1, GI 154-2, and GI 154-4 were found to be resistant to these three strains of P. syringae in this assay. Root-stock F 12-1, GI 169–15, GI 172–9, and GI 173-9 were found to be tolerant.


Molecules ◽  
2021 ◽  
Vol 26 (5) ◽  
pp. 1461
Author(s):  
Nuno Mariz-Ponte ◽  
Laura Regalado ◽  
Emil Gimranov ◽  
Natália Tassi ◽  
Luísa Moura ◽  
...  

Pseudomonas syringae pv. actinidiae (Psa) is the pathogenic agent responsible for the bacterial canker of kiwifruit (BCK) leading to major losses in kiwifruit productions. No effective treatments and measures have yet been found to control this disease. Despite antimicrobial peptides (AMPs) having been successfully used for the control of several pathogenic bacteria, few studies have focused on the use of AMPs against Psa. In this study, the potential of six AMPs (BP100, RW-BP100, CA-M, 3.1, D4E1, and Dhvar-5) to control Psa was investigated. The minimal inhibitory and bactericidal concentrations (MIC and MBC) were determined and membrane damaging capacity was evaluated by flow cytometry analysis. Among the tested AMPs, the higher inhibitory and bactericidal capacity was observed for BP100 and CA-M with MIC of 3.4 and 3.4–6.2 µM, respectively and MBC 3.4–10 µM for both. Flow cytometry assays suggested a faster membrane permeation for peptide 3.1, in comparison with the other AMPs studied. Peptide mixtures were also tested, disclosing the high efficiency of BP100:3.1 at low concentration to reduce Psa viability. These results highlight the potential interest of AMP mixtures against Psa, and 3.1 as an antimicrobial molecule that can improve other treatments in synergic action.


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