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1 E. amylovora overwinters in cankers which play an import
2 encapsulated biocontrol agent, E325, against E. amylovora, and could serve as a model for further stu
5 genic and epiphytic Erwinia species, such as E. amylovora; E. carotovora subsp. atroseptica, betavasc
9 homologs in E. carotovora, E. chrysanthemi, E. amylovora, E. herbicola, E. stewartii and E. rhaponti
11 produce antibiotics that effectively control E. amylovora, the bacterial pathogen responsible for the
13 ly reduced the induction of Hsr203 following E. amylovora challenge, further demonstrating a role for
14 tions, we depicted a clear invasion path for E. amylovora cells, from epiphytic growth on glandular t
16 ivo expression technology system to identify E. amylovora genes that are activated during infection o
19 e secretion of the main exopolysaccharide in E. amylovora, amylovoran, leading to increased biofilm f
20 hat three of the five predicted DGC genes in E. amylovora (edc genes, for Erwinia diguanylate cyclase
21 the first to describe a role for c-di-GMP in E. amylovora and suggest that downregulation of motility
25 onstrated that CsrA plays a critical role in E. amylovora virulence and suggested that negative regul
26 ringae were identified for the first time in E. amylovora and included HecA hemagglutinin family adhe
29 ce of different bacterial species, including E. amylovora, suggesting that pollinators play a role in
30 mmercially available bacterial antagonist of E. amylovora (BlightBan, Pseudomonas fluorescens A506) c
32 Erwinia species, we cloned the rsmB genes of E. amylovora (rsmB(Ea)) and E. herbicola pv. gypsophilae
33 The genome of apple, an important host of E. amylovora, has been sequenced, creating new opportuni
36 ive detection and absolute quantification of E. amylovora live cells in apple and pear cankers collec
39 ns restored pathogenicity to dspE strains of E. amylovora, although restored strains were low in viru
40 egree of genetic uniformity among strains of E. amylovora, suggesting that the pathogen has undergone
41 al proteins confirms that the hrp systems of E. amylovora and P. syringae are closely related to each
43 future, this methodology could shed light on E. amylovora population dynamics in cankers and provide
44 ation of the impact of floral microbiomes on E. amylovora colonization, and summarize the current kno
46 ations of extensive similarities between the E. amylovora and P. syringae hrp systems in pathogenesis
47 look on the genetic elements contributing to E. amylovora pathogenesis, including an exploration of t
49 ug/mL against the growth of A. tumefaciens, E. amylovora, and P. atrosepticum respectively, which we