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1                   Testing a collection of 96 B. cinerea strains showed the genetic heterogeneity of g
2 We quantified variation in lesion size of 97 B. cinerea genotypes (isolates) on six domesticated toma
3         Examination of the constituents of a B. cinerea mutant that overproduces polyketides gave suf
4                                 In addition, B. cinerea infection induced ethylene production which i
5  induced stronger activation of PDF1.2 after B. cinerea infection.
6 and JA-related defense gene expression after B. cinerea inoculation.
7 ot in a jasmonate resistant1-1 mutant, after B. cinerea infection, suggesting that P. aphidis can byp
8 ited more damage than wild type plants after B. cinerea infection, and pretreatment of plants with me
9 SV-induced resistance in Arabidopsis against B. cinerea.
10 ion of the most fungitoxic compounds against B. cinerea.
11 ibution of these pathways to defence against B. cinerea was validated through the use of multiple Ara
12 rigger the ethylene-mediated defense against B. cinerea in tomato fruits without compromising ripenin
13 ther JA responses, including defense against B. cinerea, inhibition of root elongation, and anthocyan
14 ant priming by the beneficial fungus against B. cinerea.
15  has a negative impact on resistance against B. cinerea and P. carotovorum.
16 MPK8-ERF.C1-PR' module in resistance against B. cinerea and provide new insight into the manipulation
17  developmental stages and resistance against B. cinerea was tested in fruit tissue and in progenies.
18 d chronology of the defense response against B. cinerea, highlighting the times at which signaling an
19                                        Also, B. cinerea was more aggressive than P. vulpinum and caus
20 rabidopsis Elongator subunit 2 (ELP2) alters B. cinerea-induced transcriptome reprogramming.
21 nd clock mutant strains of T. atroviride and B. cinerea, in constant light or darkness, revealed an i
22 f jasmonic acid (JA) and increased basal and B. cinerea-induced expression of the plant defensin PDF1
23 re highly susceptible to A. brassicicola and B. cinerea, whereas T-DNA insertion alleles are embryoni
24 cular dialogue between Arabidopsis cells and B. cinerea triggers major changes in host metabolism, in
25 f MYC2 fail to restore PDF1.2 expression and B. cinerea resistance in elp2, suggesting that ELP2 is r
26 sight into the biosynthesis of flavonoid and B. cinerea resistance in fruit tomatoes.
27 cate that oxalate production in A. niger and B. cinerea is solely dependent on the hydrolytic cleavag
28 se emulsion, severity levels of A. niger and B. cinerea were 60 and 73 % while the nanoemulsion treat
29 nd t18:0-P appear as key players in Pst- and B. cinerea-induced cell death and reactive oxygen specie
30 otected Arabidopsis from S. sclerotiorum and B. cinerea infections.
31 causes hypovirulence in Sclerotinia spp. and B. cinerea.
32 MPs, including resistance to P. syringae and B. cinerea, production of reactive oxygen species, callo
33 nts more susceptible to both P. syringae and B. cinerea.
34                 Here we used the Arabidopsis-B. cinerea pathosystem to test how plant host and fungal
35 opsis clathrin-coated vesicles (CCVs) around B. cinerea infection sites and the colocalization of B.
36 tence of a chemical cross-regulation between B. cinerea and T. arundinaceum and contributes to unders
37  while maintaining strong resistance to both B. cinerea and Pseudomonas syringae in Arabidopsis and t
38 rotected better against infections with both B. cinerea and A. brassicicola.
39         Induction of ATG18a and autophagy by B. cinerea was compromised in the wrky33 mutant, which i
40 re potentiated by RLs following challenge by B. cinerea or P. syringae pv tomato.
41               BOI expression was enhanced by B. cinerea and salt stress but repressed by the plant ho
42 ong the ripening-associated genes induced by B. cinerea are LePG (for polygalacturonase) and LeExp1 (
43 ses are attenuated in ripe fruit infected by B. cinerea.
44 pening influences the course of infection by B. cinerea, perhaps by changing the structure or the acc
45 haliana and tomato plants from infections by B. cinerea and V. dahliae.
46 sing a four-amino acid deletion, compromises B. cinerea-induced activation of the key immunoregulator
47            Alternative strategies to control B. cinerea are urgently needed to reduce dependence on c
48 s, and exogenous application of SA decreased B. cinerea lesion size through an NPR1-dependent mechani
49 sed genes were significantly affected during B. cinerea infection, including genes encoding proteins
50 n genes were differentially expressed during B. cinerea infection, suggesting that they are important
51 on are dynamically modulated by PMEIs during B. cinerea infection.
52 in Arabidopsis (Arabidopsis thaliana) during B. cinerea infection.
53 erlaps with COI1 and is additive to EIN2 for B. cinerea resistance.
54 sicicola resistance but additive to HUB1 for B. cinerea resistance.
55 e analysed to identify potential markers for B. cinerea infection.
56 l alcohol and 3-octanol are good markers for B. cinerea quantification and 2-octen-1-ol could be cons
57  recognizes liposomes containing GlcCer from B. cinerea, which reveals a methylated-sphingoid base st
58                       Thus, to infect fruit, B. cinerea relies on some of the processes and events th
59               Additionally, on unripe fruit, B. cinerea induces the expression of genes also expresse
60 nd economically important necrotrophic fungi B. cinerea, Alternaria brassicicola, Fusarium graminearu
61 dopsis resistance to the necrotrophic fungus B. cinerea.
62                                           In B. cinerea, fusion and infectious growth are mutually ex
63  show the existence of a functional clock in B. cinerea, which shares similar components and circuitr
64 eting the core clock-negative element FRQ in B. cinerea, but not in T. atroviride, was vital for the
65 esquiterpenes that were relatively higher in B. cinerea infected samples.
66  expression of two transferred host mRNAs in B. cinerea shows that their proteins are detrimental to
67 l proteomics analyses have been performed in B. cinerea, but they cover only 10% of the total protein
68 dicating that ELP2 is an important player in B. cinerea resistance.
69 ndicate that Sep4 plays pleiotropic roles in B. cinerea development and specifically facilities host
70 to direct inhibition, P. aphidis may inhibit B. cinerea infection via induced resistance in a manner
71 omplementation we have shown that the intact B. cinerea oahA gene restores oxalate production in an A
72                                    Moreover, B. cinerea and S. sclerotiorum mycelial growth was reduc
73                             Testing multiple B. cinerea isolates, we identified 23 separate QTL in th
74 ible as the recipient Br-0 to the necrotroph B. cinerea and to the biotroph Hyaloperonospora arabidop
75 in PA production in response to necrotrophic B. cinerea and virulent Pst DC3000 infection, but contri
76  of this study was to identify biomarkers of B. cinerea infection in sweet wines with a focus on lacc
77 ea infection sites and the colocalization of B. cinerea EV marker BcPLS1 and Arabidopsis CLATHRIN LIG
78 hyphal growth of most germinating conidia of B. cinerea and was eventually lethal to infected hyphae,
79 n, and could detect as little as 2 copies of B. cinerea DNA.
80                   The rate of development of B. cinerea disease symptoms on primary infected leaves w
81                               Germination of B. cinerea spores on sma4 mutant leaves was inhibited, a
82 -overexpressing line inhibited tip growth of B. cinerea.
83                              Infiltration of B. cinerea PGs into Arabidopsis accession Columbia induc
84 o enables genome-wide association mapping of B. cinerea Genome-wide association mapping of the pathog
85  correlated with two independent measures of B. cinerea infection levels, demonstrating that ergoster
86 nd abiotic stress and in the pathogenesis of B. cinerea.
87 ke proteins as actors in the pathogenesis of B. cinerea.
88 pathogenic fungi, the "phosphomembranome" of B. cinerea, combining the two most important signal tran
89 dentify only in infected berries proteins of B. cinerea that represent potential markers of the prese
90 inhibited germination in quiescent spores of B. cinerea In germlings, it breached the fungal plasma m
91        Critically, we identified a subset of B. cinerea genes where allelic variation was linked to a
92 at are directly linked to the suppression of B. cinerea infection.
93 1 localizes preferentially at the surface of B. cinerea.
94  gene expression is similar in both types of B. cinerea-infected plants but is repressed in Atdpl1-1
95 1 leads to dramatically reduced virulence of B. cinerea.
96 sease symptoms caused by the fungal pathogen B. cinerea in tomato and tobacco plants, and postharvest
97 sistance to the necrotrophic fungal pathogen B. cinerea, but a negative role in the SA-dependent sign
98 vealed that members of fungal plant pathogen B. cinerea BcAGO family contribute to plant infection.
99 ibility to the necrotrophic fungal pathogens B. cinerea and Alternaria brassicicola based on increase
100 ressorium formation in Ascomycota pathogens, B. cinerea, M. oryzae, Sclerotinia sclerotiorum and Moni
101                Similarly as in other plants, B. cinerea infection leads to downregulation of genes in
102 geting small molecules that not only prevent B. cinerea invasion but also have effective activity aga
103  pathogens in vitro and significantly reduce B. cinerea infection in vivo.
104                      P. aphidis also reduced B. cinerea infection, locally and systemically, in Arabi
105 stream substrates of MPK3/MPK6, also reduced B. cinerea-induced ethylene production.
106                            During noble rot, B. cinerea induced the expression of key regulators of r
107 V-1 causes hypovirulence in S. sclerotiorum, B. cinerea, and M. fructicola.
108                      Here, we show that some B. cinerea small RNAs (Bc-sRNAs) can silence Arabidopsis
109 ing bacterial EVs to plant leaves suppressed B. cinerea infection.
110  repression (EAR) motif, strongly suppresses B. cinerea-induced defense gene expression, leading to h
111 ease in necrotropic pathogen susceptibility, B. cinerea susceptibility was assessed in transgenic fru
112 or response networks may control A. thaliana-B. cinerea interaction in this population.
113                          We demonstrate that B. cinerea is able to actively absorb glucose and fructo
114                    Here, we demonstrate that B. cinerea utilizes extracellular vesicles (EVs) to secr
115 quid-cultured seedling system, we found that B. cinerea-induced ethylene biosynthesis was greatly com
116               Further analysis revealed that B. cinerea-infected Slshn3-RNAi plants are more sensitiv
117                                          The B. cinerea strain was also grown in a liquid medium for
118                                          The B. cinerea tetraspanin protein, Punchless 1 (BcPLS1), se
119 educed susceptibility to B. cinerea, and the B. cinerea dcl1 dcl2 double mutant that can no longer pr
120                    Meanwhile, BcPLS1 and the B. cinerea-secreted sRNAs are detected in purified CCVs
121 ed two immunogenic epitopes derived from the B. cinerea cell death-inducing protein BcCrh1 and used t
122 hese proteins play a significant role in the B. cinerea pathogenic cycle.
123    We analyzed the role of HA and Asp in the B. cinerea-T. arundinaceum interaction, including change
124 m results in an up-regulation of most of the B. cinerea genes involved in virulence yet the presence
125                    Genetic disruption of the B. cinerea oscillator by mutation, overexpression of BcF
126 separately and together to down-regulate the B. cinerea genes analyzed.
127  differential phenotype, suggesting that the B. cinerea clock has a more significant influence on the
128 reduced PR-1 expression but no change to the B. cinerea response.
129 he rhythmic susceptibility of Arabidopsis to B. cinerea with the enhanced susceptibility to this path
130 e to T. ni larval herbivory when compared to B. cinerea.
131 OI-RELATED GENES (BRGs), which contribute to B. cinerea resistance and the suppression of disease-ass
132 1 (coi1) and ethylene-insensitive2 (ein2) to B. cinerea, indicating that ELP2 is an important player
133 uced the susceptibility of ripening fruit to B. cinerea, as measured by fungal biomass accumulation a
134 leus, which is required for full immunity to B. cinerea Finally, we present a structural model of MOS
135  both OGs and macerozyme-induced immunity to B. cinerea in Col-0, only OGs also induced immunity in g
136 ring infection is higher and the immunity to B. cinerea is compromised in pmei10, pmei11, and pmei12
137 te to the susceptibility of wrky33 plants to B. cinerea, it is insufficient for WRKY33-mediated resis
138 he enhanced susceptibility of ssi2 plants to B. cinerea.
139 ibility of the ERF6-EAR transgenic plants to B. cinerea.
140 sed the response of the transgenic plants to B. cinerea.
141    Disease susceptibility and progression to B. cinerea and P. vulpinum increased with storage durati
142  in susceptibility occurring more rapidly to B. cinerea than P. vulpinum.
143 and acetaldehyde, while compounds related to B. cinerea were hepten-2-one and butanoic acid.
144 annins (OT) were investigated in relation to B. cinerea negative effects in grapes and musts.
145 produced and assayed for their resistance to B. cinerea and glucose transport activity.
146 expression conferred increased resistance to B. cinerea and T. ni.
147  SlERF.C1-OE lines reduced the resistance to B. cinerea attack in SlERF.C1-OE fruits.
148 STP13 contributes to the basal resistance to B. cinerea by limiting symptom development and points ou
149 pression of SlSHN3 resulted in resistance to B. cinerea infection and to X. campestris pv. vesicatori
150  CME pathway exhibit increased resistance to B. cinerea infection.
151                                Resistance to B. cinerea is compromised in the sib1 and sib2 mutants b
152 These data indicate that local resistance to B. cinerea requires ethylene-, jasmonate-, and SA-mediat
153 rtially epistatic to rst1, for resistance to B. cinerea.
154  HUB1 overexpression conferred resistance to B. cinerea.
155 ll three displayed an enhanced resistance to B. cinerea.
156 d PDF1.2, and confers enhanced resistance to B. cinerea.
157 onic acid is essential for the resistance to B. cinerea.
158 al cutin-defective mutants for resistance to B. cinerea: att1 (for aberrant induction of type three g
159 duced compared with wild type in response to B. cinerea and SA.
160 function transgenic plants or in response to B. cinerea infection increases ERF6 protein stability in
161 ive trait loci influencing plant response to B. cinerea, measured as expansion of necrotic lesions on
162 malexin than wild-type plants in response to B. cinerea.
163 l1-1 than in wild-type plants in response to B. cinerea.
164 tworks mediating the Arabidopsis response to B. cinerea.
165 ted Slshn3-RNAi plants are more sensitive to B. cinerea and produce more hydrogen peroxide than wild-
166 e bccrh1 gene exhibit reduced sensitivity to B. cinerea, suggesting a potential use of the BcCrh1 pro
167 efect in a response pathway more specific to B. cinerea.
168 s plants show differential susceptibility to B. cinerea depending on the time of day of inoculation.
169              The decreased susceptibility to B. cinerea following inoculation at subjective dawn was
170       We show that reduced susceptibility to B. cinerea is dependent specifically on the accumulation
171 a suggest that PA-mediated susceptibility to B. cinerea is linked to interference with the functions
172 f SlERF.C1 increased fruit susceptibility to B. cinerea with no effect on ripening process, while ove
173 o1 mutant exhibits reduced susceptibility to B. cinerea, and the B. cinerea dcl1 dcl2 double mutant t
174  of SlMPK8 increased fruit susceptibility to B. cinerea, whereas overexpression enhanced resistance w
175 2 both exhibited decreased susceptibility to B. cinerea.
176 for genotypes with reduced susceptibility to B. cinerea.
177 ock in driving time-of-day susceptibility to B. cinerea.
178 free radicals, and reduced susceptibility to B. cinerea.
179 n markedly increased plant susceptibility to B. cinerea; the effect of low R:FR was (1) independent o
180      In bos3, the mutant most susceptible to B. cinerea and with the highest expression of PR-1, remo
181            The bos2 mutant is susceptible to B. cinerea but retains wild-type levels of resistance to
182 th the S-enantiomer were more susceptible to B. cinerea infection than to T. ni larval herbivory, whi
183 1 mutant leaves were normally susceptible to B. cinerea infection, a double ein2 npr1 mutant was sign
184 sgenic tomato lines were more susceptible to B. cinerea than the wild-type plants; however, responses
185 stant to P. syringae but more susceptible to B. cinerea than wild-type plants.
186 tibility of the ySpdSyn transgenic tomato to B. cinerea was associated with down-regulation of gene t
187 espond faster and in a more effective way to B. cinerea invasion.
188 of abscisic acid (ABA) in resistance towards B. cinerea 2100.
189 by Arabidopsis to resist CW degradation upon B. cinerea infection.
190 ferential transcriptional reprogramming upon B. cinerea infection.
191 OT and all the virulence genes analyzed when B. cinerea was grown alone.
192 ntification of lab-inoculated samples, while B. cinerea antigen detection is more suitable for natura
193  STP13 was induced in leaves challenged with B. cinerea.
194  must obtained by inoculation of grapes with B. cinerea strain 213.
195 s and transcriptomes of leaves infected with B. cinerea mutants with reduced pectinolytic activity bu
196       Macerozyme treatment or infection with B. cinerea released less soluble uronic acid, likely ref
197 sed camalexin production upon infection with B. cinerea.
198 matoes with this coating and inoculated with B. cinerea showed a significant decrease in fungal growt

 
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