ライフサイエンスコーパス: B. cinerea

1 Examination of the constituents of a B. cinerea mutant that overproduces polyketides gave suf

2 induced stronger activation of PDF1.2 after B. cinerea infection.

3 and JA-related defense gene expression after B. cinerea inoculation.

4 ot in a jasmonate resistant1-1 mutant, after B. cinerea infection, suggesting that P. aphidis can byp

5 ited more damage than wild type plants after B. cinerea infection, and pretreatment of plants with me

6 SV-induced resistance in Arabidopsis against B. cinerea.

7 ion of the most fungitoxic compounds against B. cinerea.

8 ibution of these pathways to defence against B. cinerea was validated through the use of multiple Ara

9 has a negative impact on resistance against B. cinerea and P. carotovorum.

10 d chronology of the defense response against B. cinerea, highlighting the times at which signaling an

11 rabidopsis Elongator subunit 2 (ELP2) alters B. cinerea-induced transcriptome reprogramming.

12 f jasmonic acid (JA) and increased basal and B. cinerea-induced expression of the plant defensin PDF1

13 re highly susceptible to A. brassicicola and B. cinerea, whereas T-DNA insertion alleles are embryoni

14 cular dialogue between Arabidopsis cells and B. cinerea triggers major changes in host metabolism, in

15 f MYC2 fail to restore PDF1.2 expression and B. cinerea resistance in elp2, suggesting that ELP2 is r

16 cate that oxalate production in A. niger and B. cinerea is solely dependent on the hydrolytic cleavag

17 nd t18:0-P appear as key players in Pst- and B. cinerea-induced cell death and reactive oxygen specie

18 causes hypovirulence in Sclerotinia spp. and B. cinerea.

19 nts more susceptible to both P. syringae and B. cinerea.

20 tence of a chemical cross-regulation between B. cinerea and T. arundinaceum and contributes to unders

21 rotected better against infections with both B. cinerea and A. brassicicola.

22 Induction of ATG18a and autophagy by B. cinerea was compromised in the wrky33 mutant, which i

23 re potentiated by RLs following challenge by B. cinerea or P. syringae pv tomato.

24 BOI expression was enhanced by B. cinerea and salt stress but repressed by the plant ho

25 ong the ripening-associated genes induced by B. cinerea are LePG (for polygalacturonase) and LeExp1 (

26 ses are attenuated in ripe fruit infected by B. cinerea.

27 pening influences the course of infection by B. cinerea, perhaps by changing the structure or the acc

28 sing a four-amino acid deletion, compromises B. cinerea-induced activation of the key immunoregulator

29 s, and exogenous application of SA decreased B. cinerea lesion size through an NPR1-dependent mechani

30 on are dynamically modulated by PMEIs during B. cinerea infection.

31 in Arabidopsis (Arabidopsis thaliana) during B. cinerea infection.

32 erlaps with COI1 and is additive to EIN2 for B. cinerea resistance.

33 sicicola resistance but additive to HUB1 for B. cinerea resistance.

34 Thus, to infect fruit, B. cinerea relies on some of the processes and events th

35 Additionally, on unripe fruit, B. cinerea induces the expression of genes also expresse

36 nd economically important necrotrophic fungi B. cinerea, Alternaria brassicicola, Fusarium graminearu

37 dopsis resistance to the necrotrophic fungus B. cinerea.

38 show the existence of a functional clock in B. cinerea, which shares similar components and circuitr

39 dicating that ELP2 is an important player in B. cinerea resistance.

40 ndicate that Sep4 plays pleiotropic roles in B. cinerea development and specifically facilities host

41 to direct inhibition, P. aphidis may inhibit B. cinerea infection via induced resistance in a manner

42 omplementation we have shown that the intact B. cinerea oahA gene restores oxalate production in an A

43 Testing multiple B. cinerea isolates, we identified 23 separate QTL in th

44 ible as the recipient Br-0 to the necrotroph B. cinerea and to the biotroph Hyaloperonospora arabidop

45 in PA production in response to necrotrophic B. cinerea and virulent Pst DC3000 infection, but contri

46 hyphal growth of most germinating conidia of B. cinerea and was eventually lethal to infected hyphae,

47 n, and could detect as little as 2 copies of B. cinerea DNA.

48 The rate of development of B. cinerea disease symptoms on primary infected leaves w

49 Germination of B. cinerea spores on sma4 mutant leaves was inhibited, a

50 -overexpressing line inhibited tip growth of B. cinerea.

51 Infiltration of B. cinerea PGs into Arabidopsis accession Columbia induc

52 nd abiotic stress and in the pathogenesis of B. cinerea.

53 dentify only in infected berries proteins of B. cinerea that represent potential markers of the prese

54 gene expression is similar in both types of B. cinerea-infected plants but is repressed in Atdpl1-1

55 sistance to the necrotrophic fungal pathogen B. cinerea, but a negative role in the SA-dependent sign

56 ibility to the necrotrophic fungal pathogens B. cinerea and Alternaria brassicicola based on increase

57 pathogens in vitro and significantly reduce B. cinerea infection in vivo.

58 P. aphidis also reduced B. cinerea infection, locally and systemically, in Arabi

59 stream substrates of MPK3/MPK6, also reduced B. cinerea-induced ethylene production.

60 During noble rot, B. cinerea induced the expression of key regulators of r

61 Here, we show that some B. cinerea small RNAs (Bc-sRNAs) can silence Arabidopsis

62 repression (EAR) motif, strongly suppresses B. cinerea-induced defense gene expression, leading to h

63 ease in necrotropic pathogen susceptibility, B. cinerea susceptibility was assessed in transgenic fru

64 or response networks may control A. thaliana-B. cinerea interaction in this population.

65 We demonstrate that B. cinerea is able to actively absorb glucose and fructo

66 quid-cultured seedling system, we found that B. cinerea-induced ethylene biosynthesis was greatly com

67 Further analysis revealed that B. cinerea-infected Slshn3-RNAi plants are more sensitiv

68 educed susceptibility to B. cinerea, and the B. cinerea dcl1 dcl2 double mutant that can no longer pr

69 We analyzed the role of HA and Asp in the B. cinerea-T. arundinaceum interaction, including change

70 m results in an up-regulation of most of the B. cinerea genes involved in virulence yet the presence

71 Genetic disruption of the B. cinerea oscillator by mutation, overexpression of BcF

72 separately and together to down-regulate the B. cinerea genes analyzed.

73 reduced PR-1 expression but no change to the B. cinerea response.

74 he rhythmic susceptibility of Arabidopsis to B. cinerea with the enhanced susceptibility to this path

75 OI-RELATED GENES (BRGs), which contribute to B. cinerea resistance and the suppression of disease-ass

76 1 (coi1) and ethylene-insensitive2 (ein2) to B. cinerea, indicating that ELP2 is an important player

77 uced the susceptibility of ripening fruit to B. cinerea, as measured by fungal biomass accumulation a

78 leus, which is required for full immunity to B. cinerea Finally, we present a structural model of MOS

79 both OGs and macerozyme-induced immunity to B. cinerea in Col-0, only OGs also induced immunity in g

80 ring infection is higher and the immunity to B. cinerea is compromised in pmei10, pmei11, and pmei12

81 te to the susceptibility of wrky33 plants to B. cinerea, it is insufficient for WRKY33-mediated resis

82 ibility of the ERF6-EAR transgenic plants to B. cinerea.

83 sed the response of the transgenic plants to B. cinerea.

84 he enhanced susceptibility of ssi2 plants to B. cinerea.

85 produced and assayed for their resistance to B. cinerea and glucose transport activity.

86 expression conferred increased resistance to B. cinerea and T. ni.

87 STP13 contributes to the basal resistance to B. cinerea by limiting symptom development and points ou

88 pression of SlSHN3 resulted in resistance to B. cinerea infection and to X. campestris pv. vesicatori

89 Resistance to B. cinerea is compromised in the sib1 and sib2 mutants b

90 These data indicate that local resistance to B. cinerea requires ethylene-, jasmonate-, and SA-mediat

91 ll three displayed an enhanced resistance to B. cinerea.

92 d PDF1.2, and confers enhanced resistance to B. cinerea.

93 onic acid is essential for the resistance to B. cinerea.

94 rtially epistatic to rst1, for resistance to B. cinerea.

95 HUB1 overexpression conferred resistance to B. cinerea.

96 al cutin-defective mutants for resistance to B. cinerea: att1 (for aberrant induction of type three g

97 duced compared with wild type in response to B. cinerea and SA.

98 function transgenic plants or in response to B. cinerea infection increases ERF6 protein stability in

99 ive trait loci influencing plant response to B. cinerea, measured as expansion of necrotic lesions on

100 malexin than wild-type plants in response to B. cinerea.

101 l1-1 than in wild-type plants in response to B. cinerea.

102 tworks mediating the Arabidopsis response to B. cinerea.

103 ted Slshn3-RNAi plants are more sensitive to B. cinerea and produce more hydrogen peroxide than wild-

104 efect in a response pathway more specific to B. cinerea.

105 s plants show differential susceptibility to B. cinerea depending on the time of day of inoculation.

106 The decreased susceptibility to B. cinerea following inoculation at subjective dawn was

107 We show that reduced susceptibility to B. cinerea is dependent specifically on the accumulation

108 a suggest that PA-mediated susceptibility to B. cinerea is linked to interference with the functions

109 o1 mutant exhibits reduced susceptibility to B. cinerea, and the B. cinerea dcl1 dcl2 double mutant t

110 ock in driving time-of-day susceptibility to B. cinerea.

111 free radicals, and reduced susceptibility to B. cinerea.

112 2 both exhibited decreased susceptibility to B. cinerea.

113 n markedly increased plant susceptibility to B. cinerea; the effect of low R:FR was (1) independent o

114 In bos3, the mutant most susceptible to B. cinerea and with the highest expression of PR-1, remo

115 The bos2 mutant is susceptible to B. cinerea but retains wild-type levels of resistance to

116 1 mutant leaves were normally susceptible to B. cinerea infection, a double ein2 npr1 mutant was sign

117 sgenic tomato lines were more susceptible to B. cinerea than the wild-type plants; however, responses

118 stant to P. syringae but more susceptible to B. cinerea than wild-type plants.

119 tibility of the ySpdSyn transgenic tomato to B. cinerea was associated with down-regulation of gene t

120 espond faster and in a more effective way to B. cinerea invasion.

121 of abscisic acid (ABA) in resistance towards B. cinerea 2100.

122 by Arabidopsis to resist CW degradation upon B. cinerea infection.

123 ferential transcriptional reprogramming upon B. cinerea infection.

124 OT and all the virulence genes analyzed when B. cinerea was grown alone.

125 STP13 was induced in leaves challenged with B. cinerea.

126 Macerozyme treatment or infection with B. cinerea released less soluble uronic acid, likely ref

127 matoes with this coating and inoculated with B. cinerea showed a significant decrease in fungal growt