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1 resistant to a necrotrophic fungal pathogen, Botrytis cinerea.
2 yringae and the necrotrophic fungal pathogen Botrytis cinerea.
3 protection against the fungal phytopathogen Botrytis cinerea.
4 nfection by the necrotrophic fungal pathogen Botrytis cinerea.
5 esponses to the necrotrophic fungal pathogen Botrytis cinerea.
6 d in resistance to the necrotrophic pathogen Botrytis cinerea.
7 noculation sites of Penicillium expansum and Botrytis cinerea.
8 al immunity against the fungal phytopathogen Botrytis cinerea.
9 behaviour of the inclusion complexes against Botrytis cinerea.
10 cearum, but not to the necrotrophic pathogen Botrytis cinerea.
11 ns of ripe grape (Vitis vinifera) berries by Botrytis cinerea.
12 ibility to the necrotrophic fungal pathogen, Botrytis cinerea.
13 opsis mutant wrky33 is highly susceptible to Botrytis cinerea.
14 SsPV1 can infect and cause hypovirulence in Botrytis cinerea.
15 irulence of the necrotrophic fungal pathogen Botrytis cinerea.
16 d protection against the necrotrophic fungus Botrytis cinerea.
17 s with its plant host and the plant pathogen Botrytis cinerea.
18 sistance to the necrotrophic fungal pathogen Botrytis cinerea.
19 ceptible than wild-type plants to the fungus Botrytis cinerea.
20 le to S. sclerotiorum and the related fungus Botrytis cinerea.
21 Aspergillus niger, Trichoderma harzianum and Botrytis cinerea.
22 nd against the necrotrophic fungal pathogen, Botrytis cinerea.
23 a arabidopsidis, and the necrotrophic fungus Botrytis cinerea.
24 when seedlings were infected with the fungus Botrytis cinerea.
25 nfection by the necrotrophic fungal pathogen Botrytis cinerea.
26 l for defense toward the necrotrophic fungus Botrytis cinerea.
27 ae pv. tomato DC3000 and the fungal pathogen Botrytis cinerea.
28 ance toward the necrotrophic fungal pathogen Botrytis cinerea.
29 trongly induced by the necrotrophic pathogen Botrytis cinerea.
30 bidopsis by the necrotrophic fungal pathogen Botrytis cinerea.
31 larvae and the necrotrophic fungal pathogen Botrytis cinerea.
32 susceptibility to the necrotrophic pathogen Botrytis cinerea.
33 onset of disease symptoms when infected with Botrytis cinerea.
34 ces foliar resistance to the fungal pathogen Botrytis cinerea.
35 ptibility to necrotrophic pathogens, such as Botrytis cinerea.
36 antly increased resistance toward gray mold (Botrytis cinerea), a pathogen responsible for major loss
38 ified SsPV1/WF-1 virions into strain KY-1 of Botrytis cinerea also resulted in reductions in virulenc
39 esistance to several plant pathogens (namely Botrytis cinerea, Alternaria brassicicola and Golovinomy
40 ced susceptibility to the necrotrophic fungi Botrytis cinerea and Alternaria brassicicola as well as
41 ibility to the necrotrophic fungal pathogens Botrytis cinerea and Alternaria brassicicola concomitant
42 istance to the necrotrophic fungal pathogens Botrytis cinerea and Alternaria brassicicola in the Noss
43 ibility to the necrotrophic fungal pathogens Botrytis cinerea and Alternaria brassicicola, whereas HU
47 eased susceptibility to the pathogenic fungi Botrytis cinerea and Alternaria brassisicola Both PAMPs
48 ined for responses to the fungal necrotrophs Botrytis cinerea and Alternaria solani, bacterial pathog
49 ed susceptibility to the necrotrophic fungus Botrytis cinerea and an increased tolerance to the biotr
50 increased resistance to the fungal pathogens Botrytis cinerea and Bipolaris sorokiniana but not to th
51 ease resistance to the necrotrophic pathogen Botrytis cinerea and contributes to basal defense induce
53 d defenses against the necrotrophic pathogen Botrytis cinerea and for the shade-triggered increased s
55 xpression of defense genes and resistance to Botrytis cinerea and Pectobacterium carotovorum infectio
56 tes JA-mediated resistance to the necrotroph Botrytis cinerea and susceptibility to the hemibiotroph
57 response to the necrotrophic foliar pathogen Botrytis cinerea and the biotrophic bacterial pathogen X
58 reased resistance to the necrotrophic fungus Botrytis cinerea and the caterpillar Mamestra brassicae
59 sistance to the necrotrophic fungal pathogen Botrytis cinerea and their genetic control are poorly un
60 to susceptibility to the necrotrophic fungus Botrytis cinerea and to feeding by larvae of tobacco hor
62 ed susceptibility to the necrotrophic fungus Botrytis cinerea, and increased sensitivity to salt and
63 The pectin matrix is the main CW target of Botrytis cinerea, and pectin methylesterification status
64 efense responses against the fungal pathogen Botrytis cinerea, and thus we conclude that the regulati
66 cognizes several PGs from the plant pathogen Botrytis cinerea as well as one from the saprotroph Aspe
71 chitinase activity and induced expression of Botrytis cinerea BOT genes, although their total antagon
72 exhibit tolerance to the necrotrophic fungus Botrytis cinerea but susceptibility to the hemibiotrophi
73 tibility to the necrotrophic fungal pathogen Botrytis cinerea, but showed normal responses to virulen
74 -enolide (1) was assigned to a metabolite of Botrytis cinerea, but the spectra of several synthetic a
75 T2 gene from the necrotrophic plant pathogen Botrytis cinerea, catalyzes the multistep cyclization of
76 including Pst-AvrRpt2, Dickeya dadantii, and Botrytis cinerea Characterization of the redox status de
77 ption of SEP4 in the plant grey mould fungus Botrytis cinerea completely blocked IFS formation and ab
78 dopsis resistance to the necrotrophic fungus Botrytis cinerea, consistent with substantial upregulati
80 Such sRNA effectors are mostly produced by Botrytis cinerea Dicer-like protein 1 (Bc-DCL1) and Bc-D
81 9 and 3310 mg/L against Rhizopus stolonifer, Botrytis cinerea, Fusarium oxysporum and Colletotrichum
83 e markers induced by the necrotrophic fungus Botrytis cinerea, including the genes that encode the tr
84 quired for resistance to the fungal pathogen Botrytis cinerea, indicating that NHO1 is not limited to
85 oligosaccharides (PDOs) in three regions of Botrytis cinerea-infected tomato fruit tissue is describ
86 lly regulated during abiotic stresses during Botrytis cinerea infection or after benzothiadiazole and
87 Transgenic plants were more resistant to Botrytis cinerea infection than wild type, possibly as a
88 are upregulated coordinately in response to Botrytis cinerea infection, but through separate signal
89 with AA exhibited reduced susceptibility to Botrytis cinerea infection, confirming AA signaling in o
94 opsis, resistance to the necrotrophic fungus Botrytis cinerea is conferred by ethylene via poorly und
95 nt defense against the necrotrophic pathogen Botrytis cinerea is primarily quantitative and genetical
101 hocyanin accumulation, and susceptibility to Botrytis cinerea, one of the most important postharvest
102 ter are more resistant to the phytopathogens Botrytis cinerea, Pectobacterium carotovorum, and Pseudo
104 ee agriculturally important plant pathogens (Botrytis cinerea, Pseudomonas syringae, and Fusarium oxy
105 netic analysis revealed flg22-induced PTI to Botrytis cinerea requires BIK1, EIN2, and HUB1 but not g
106 tered in response to the necrotrophic fungus Botrytis cinerea revealed decreases in the levels of pho
107 resistance against the necrotrophic fungus, Botrytis cinerea The induced resistance was enhanced in
108 tial for immunity to the necrotrophic fungus Botrytis cinerea The mos7-1 mutation, causing a four-ami
110 After infection with Pseudomonas syringae or Botrytis cinerea, the expression of genes regulated by b
111 ighlighted by an increased susceptibility to Botrytis cinerea This process was accompanied by an over
112 , the circadian system of the plant pathogen Botrytis cinerea to assess if such oscillatory machinery
114 dopsis thaliana with the necrotrophic fungus Botrytis cinerea using millicell culture insert, that en
118 hytopathogenic fungi, Fusarium oxysporum and Botrytis cinerea, were chosen to examine the antifungal
119 tibility to infection by the fungal pathogen Botrytis cinerea, which was associated with much stronge
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