ライフサイエンスコーパス: necrotrophic

1 Both necrotrophic and biotrophic fungi have larger genomes th

2 Necrotrophic and biotrophic pathogens are resisted by di

3 s increased susceptibility of plants against necrotrophic attackers by suppressing the jasmonic acid-

4 the increase in PA production in response to necrotrophic B. cinerea and virulent Pst DC3000 infectio

5 tomato DC3000 and for susceptibility to the necrotrophic bacteria Erwinia caratovora pv.

6 ency was most harmful to the host during the necrotrophic colonization phase.

7 hormonal network typically activated by both necrotrophic (ET/JA) and biotrophic (SA) pathogens suppo

8 vora is a devastating plant pathogen causing necrotrophic fire blight disease of apple, pear, and oth

9 n the tomato plant's defense response to the necrotrophic foliar pathogen Botrytis cinerea and the bi

10 sucrose and at the expense of starch during necrotrophic fungal growth.

11 thus limiting the defense function of UPI to necrotrophic fungal infection and insect herbivory.

12 cumulated JA in response to infection by the necrotrophic fungal pathogen Alternaria brassicicola.

13 host plant during successful infection by a necrotrophic fungal pathogen and the resistance response

14 ed JA production and plant resistance to the necrotrophic fungal pathogen B. cinerea, but a negative

15 chanisms involved in plant resistance to the necrotrophic fungal pathogen Botrytis cinerea and their

16 nts displayed enhanced susceptibility to the necrotrophic fungal pathogen Botrytis cinerea, but showe

17 phagosomes are induced in Arabidopsis by the necrotrophic fungal pathogen Botrytis cinerea.

18 against herbivorous M. sexta larvae and the necrotrophic fungal pathogen Botrytis cinerea.

19 terial pathogen Pseudomonas syringae and the necrotrophic fungal pathogen Botrytis cinerea.

20 were highly susceptible to infection by the necrotrophic fungal pathogen Botrytis cinerea.

21 mutants impaired in defense responses to the necrotrophic fungal pathogen Botrytis cinerea.

22 tivity is important for the virulence of the necrotrophic fungal pathogen Botrytis cinerea.

23 efense gene expression and resistance to the necrotrophic fungal pathogen Botrytis cinerea.

24 dopsis thaliana leaf during infection by the necrotrophic fungal pathogen Botrytis cinerea.

25 wa2 displayed increased tolerance toward the necrotrophic fungal pathogen Botrytis cinerea.

26 e of wheat (Triticum aestivum) leaves to the necrotrophic fungal pathogen Mycosphaerella graminicola

27 ants also exhibit enhanced resistance to the necrotrophic fungal pathogen Rhizoctonia solani.

28 culture filtrate elicitor1 (SCFE1) from the necrotrophic fungal pathogen Sclerotinia sclerotiorum th

29 The necrotrophic fungal pathogen Sclerotinia trifoliorum exh

30 Alternaria brassicicola is an important, necrotrophic fungal pathogen that causes black spot dise

31 y, the sma4 mutant was highly resistant to a necrotrophic fungal pathogen, Botrytis cinerea.

32 adian clock influences susceptibility to the necrotrophic fungal pathogen, Botrytis cinerea.

33 es, caterpillars and aphids, and against the necrotrophic fungal pathogen, Botrytis cinerea.

34 tivation of PGN results in susceptibility to necrotrophic fungal pathogens as well as hypersensitivit

35 phagy exhibit enhanced susceptibility to the necrotrophic fungal pathogens B. cinerea and Alternaria

36 cichoracearum but enhanced resistance to the necrotrophic fungal pathogens Botrytis cinerea and Alter

37 of HUB1 show increased susceptibility to the necrotrophic fungal pathogens Botrytis cinerea and Alter

38 gnaling conferred enhanced resistance to the necrotrophic fungal pathogens Botrytis cinerea and Alter

39 factor cause enhanced susceptibility to the necrotrophic fungal pathogens Botrytis cinerea and Alter

40 FENSIN1.2 (PDF1.2) and for resistance to the necrotrophic fungal pathogens Botrytis cinerea and Alter

41 sive genes and compromised resistance to the necrotrophic fungal pathogens Botrytis cinerea and Alter

42 tion of BIK1 causes severe susceptibility to necrotrophic fungal pathogens but enhances resistance to

43 es conferred heritable resistance to several necrotrophic fungal pathogens, suggesting that disease d

44 echanisms of susceptibility, particularly to necrotrophic fungal pathogens.

45 other hand, increases resistance to the two necrotrophic fungal pathogens.

46 d cell death-eliciting toxin produced by the necrotrophic fungal plant pathogen Fusarium moniliforme,

47 d shared defense mechanism for resistance to necrotrophic fungi and herbivorous insects.

48 the agronomically and economically important necrotrophic fungi B. cinerea, Alternaria brassicicola,

49 ele displayed enhanced susceptibility to the necrotrophic fungi Botrytis cinerea and Alternaria brass

50 ation of disease responses to biotrophic and necrotrophic fungi in that it antagonizes salicylic acid

51 le of SA-dependent defense responses against necrotrophic fungi is currently unclear.

52 Plant resistance to necrotrophic fungi is regulated by a complex set of sign

53 th regulatory roles in plant defense against necrotrophic fungi most likely through modulation of gen

54 Plants challenged by pathogens, especially necrotrophic fungi such as Botrytis cinerea, produce hig

55 As play in plant defense against insects and necrotrophic fungi, (2) argue for a reassessment of sign

56 nse, generally associated with resistance to necrotrophic fungi, is attenuated in the bik1 mutant bas

57 e modulate the resistance of hub1 mutants to necrotrophic fungi.

58 ant defenses against herbivorous insects and necrotrophic fungi.

59 defence against insect herbivores and foliar necrotrophic fungi.

60 of MAMP-triggered immunity in resistance to necrotrophic fungi.

61 y regulating SA/JA/ET-mediated resistance to necrotrophic fungi.

62 s (ROS) is critical for pathogenicity in the necrotrophic fungus Alternaria alternata.

63 ingly, the elevated resistance of gai to the necrotrophic fungus Alternaria brassicicola and suscepti

64 iggered immunity and immune responses to the necrotrophic fungus Alternaria brassicicola and the bact

65 ble genes and enhanced susceptibility to the necrotrophic fungus Alternaria brassicicola.

66 production and Arabidopsis resistance to the necrotrophic fungus B. cinerea.

67 s present an increased susceptibility to the necrotrophic fungus Botrytis cinerea and an increased to

68 ence (BOI RNAi) were more susceptible to the necrotrophic fungus Botrytis cinerea and less tolerant t

69 e expression and increased resistance to the necrotrophic fungus Botrytis cinerea and the caterpillar

70 RNAi) increases tomato susceptibility to the necrotrophic fungus Botrytis cinerea and to feeding by l

71 Atdpl1 mutants exhibit tolerance to the necrotrophic fungus Botrytis cinerea but susceptibility

72 In Arabidopsis, resistance to the necrotrophic fungus Botrytis cinerea is conferred by eth

73 of lipid species altered in response to the necrotrophic fungus Botrytis cinerea revealed decreases

74 Nup88/MOS7 is essential for immunity to the necrotrophic fungus Botrytis cinerea The mos7-1 mutation

75 interaction of Arabidopsis thaliana with the necrotrophic fungus Botrytis cinerea using millicell cul

76 sion show an increased susceptibility to the necrotrophic fungus Botrytis cinerea, and increased sens

77 of PS improves Arabidopsis resistance to the necrotrophic fungus Botrytis cinerea, consistent with su

78 expression of defense markers induced by the necrotrophic fungus Botrytis cinerea, including the gene

79 defense responses and protection against the necrotrophic fungus Botrytis cinerea.

80 cete Hyaloperonospora arabidopsidis, and the necrotrophic fungus Botrytis cinerea.

81 r WRKY33 is essential for defense toward the necrotrophic fungus Botrytis cinerea.

82 among victorin (an effector produced by the necrotrophic fungus Cochliobolus victoriae), TRX-h5 (a d

83 findings suggest an explanation for why the necrotrophic fungus Gibberella fujikuroi, causal agent o

84 We observe that the lesions produced by this necrotrophic fungus on Arabidopsis leaves are smaller wh

85 the enhanced susceptibility of agb1-2 to the necrotrophic fungus Plectosphaerella cucumerina BMM (PcB

86 sis (Arabidopsis thaliana) resistance to the necrotrophic fungus Plectosphaerella cucumerina.

87 allenge by a hemi-biotrophic bacterium and a necrotrophic fungus, as well as in the growth response t

88 pretreatment induced resistance against the necrotrophic fungus, Botrytis cinerea The induced resist

89 ve to aos, opr3 has enhanced resistance to a necrotrophic fungus.

90 ng fructan metabolites, during the switch to necrotrophic growth and reproduction.

91 We hypothesize that the switch to necrotrophic growth enables the fungus to evade the effe

92 ase in the penetrated epidermis cell, before necrotrophic growth is initiated upon further host colon

93 le during the transition from symptomless to necrotrophic growth of Septoria.

94 m Phytophthora that are expressed during the necrotrophic growth phase, as well as programmed cell de

95 host cells followed by a rapid transition to necrotrophic growth resulting in disease lesions.

96 g of host transcription marks this switch to necrotrophic growth.

97 pressorium on the cuticle and biotrophic and necrotrophic hyphae in its host.

98 ophic hyphae was unaffected in RNAi strains, necrotrophic hyphae showed severe distortions.

99 all rigidity in appressoria and fast-growing necrotrophic hyphae, its rigorous downregulation during

100 re detected in cell walls of appressoria and necrotrophic hyphae.

101 er, the AtECS plants exhibited resistance to necrotrophic infection and salt stress, while the pad2-1

102 es can result in impaired plant tolerance to necrotrophic infection or abiotic stress.

103 nses by switching from a hemibiotrophic to a necrotrophic infection program, thereby gaining an advan

104 -HAC boosts JA-dependent defenses during the necrotrophic infection stage of F. graminearum but suppr

105 and senescence, the pathogens switch to the necrotrophic lifestyle and cause decay.

106 ate the transition from the quiescent to the necrotrophic lifestyle.

107 ls during the transition from biotrophy to a necrotrophic lifestyle.

108 host plant and later switch to a destructive necrotrophic lifestyle.

109 merina alternates between hemibiotrophic and necrotrophic lifestyles, depending on initial spore dens

110 abidopsis thaliana) immune responses against necrotrophic microorganisms via a SA-independent mechani

111 nse, rendered plants more susceptible to the necrotrophic pathogen Alternaria brassicicola by suppres

112 novel components of plant immunity toward a necrotrophic pathogen and provides mechanistic insights

113 ols broad-spectrum disease resistance to the necrotrophic pathogen Botrytis cinerea and contributes t

114 equired for JA-mediated defenses against the necrotrophic pathogen Botrytis cinerea and for the shade

115 tudy suggests that plant defense against the necrotrophic pathogen Botrytis cinerea is primarily quan

116 SIB2 are rapidly and strongly induced by the necrotrophic pathogen Botrytis cinerea.

117 ociated with increased susceptibility to the necrotrophic pathogen Botrytis cinerea.

118 ponsive gene PDF1.2 and in resistance to the necrotrophic pathogen Botrytis cinerea.

119 Golovinomyces cichoracearum, but not to the necrotrophic pathogen Botrytis cinerea.

120 was sufficient to change the host range of a necrotrophic pathogen but not a hemibiotroph or saprotro

121 ce to pitch canker, a disease incited by the necrotrophic pathogen Fusarium circinatum.

122 t be advantageous to the plant by preventing necrotrophic pathogen growth in tissues undergoing PCD.

123 ns of wheat (Triticum aestivum), including a necrotrophic pathogen of barley, a hemibiotrophic pathog

124 Stagonospora nodorum is a major necrotrophic pathogen of wheat that causes the diseases

125 Against infection by the necrotrophic pathogen Plectosphaerella cucumerina, nrpe1

126 s required to restrict the spread of another necrotrophic pathogen, Alternaria brassicicola, suggesti

127 tibility to Alternaria brassicicola, another necrotrophic pathogen, suggesting a broader role for the

128 by necrosis that occurred in response to the necrotrophic pathogen.

129 way that enables the plant to defend against necrotrophic pathogens and herbivorous insects apparentl

130 Necrotrophic pathogens are important plant pathogens tha

131 Necrotrophic pathogens are notorious for their aggressiv

132 While necrotrophic pathogens are sensitive to jasmonic acid (J

133 Because wound-invading necrotrophic pathogens are vulnerable to biocontrol, ant

134 In contrast, necrotrophic pathogens benefit from host cell death, so

135 Few studies of quantitative resistance to necrotrophic pathogens have used large plant mapping pop

136 nhance understanding of host manipulation by necrotrophic pathogens in causing disease.

137 -dependent defence responses engaged against necrotrophic pathogens in root tissue.

138 derstanding of the plant defense response to necrotrophic pathogens is limited.

139 Genetic resistance to disease incited by necrotrophic pathogens is not well understood in plants.

140 This work suggests that these necrotrophic pathogens may thrive by subverting the resi

141 cells, whereas JA activates defense against necrotrophic pathogens that kill host cells for nutritio

142 ssociated PCD could leave them vulnerable to necrotrophic pathogens that thrive on dead host cells.

143 No elevated resistance toward herbivores or necrotrophic pathogens was detected for cpk28 plants, ei

144 Plant resistance against necrotrophic pathogens with a broad host range is comple

145 ant role in plant defense, especially toward necrotrophic pathogens, and highlight a novel connection

146 by a dramatic increase in susceptibility to necrotrophic pathogens, such as Botrytis cinerea.

147 rsely, ros1 displayed enhanced resistance to necrotrophic pathogens, which was not associated with in

148 plays a critical role in plant resistance to necrotrophic pathogens.

149 on factor that is required for resistance to necrotrophic pathogens.

150 ctivators of WRKY33 in plant defense against necrotrophic pathogens.

151 hance our understanding of plant immunity to necrotrophic pathogens.

152 the regulation of plant defense responses to necrotrophic pathogens.

153 hways mediating responses to P. syringae and necrotrophic pathogens.

154 nses to resistance to several biotrophic and necrotrophic pathogens.

155 phic pathogen without becoming vulnerable to necrotrophic pathogens.

156 ar from being understood, especially against necrotrophic pathogens.

157 dentified a role for TGA3 in defense against necrotrophic pathogens.

158 rky33 mutant, which is highly susceptible to necrotrophic pathogens.

159 factor is important for plant resistance to necrotrophic pathogens; therefore, elucidation of its fu

160 hemibiotrophic Pseudomonas syringae and the necrotrophic Pectobacterium carotovorum bacteria.

161 host tissue asymptomatically, followed by a necrotrophic phase, during which host-cell death is indu

162 at the switch between the biotrophic and the necrotrophic phases.

163 Here we characterized a CP (SsCP1) from the necrotrophic phytopathogen Sclerotinia sclerotiorum.

164 ynthase, encoded by the BcBOT2 gene from the necrotrophic plant pathogen Botrytis cinerea, catalyzes

165 pecies and diversifying selection within the necrotrophic plant pathogen ecological niche.

166 brassicicola is a successful saprophyte and necrotrophic plant pathogen.

167 re caused by biotrophic, hemibiotrophic, and necrotrophic plant pathogens.

168 l death as a component of diseases caused by necrotrophic plant pathogens.

169 e resistance toward (hemi)biotrophic but not necrotrophic rice pathogens.

170 The diversity of virulence strategies in necrotrophic species corresponds to multifaceted host im

171 ession of effector-triggered necrosis at the necrotrophic stage by an NLR receptor in plants.

172 transition from the biotrophic stage to the necrotrophic stage in disease symptom expression are mai

173 stabilizes APIP5 to prevent necrosis at the necrotrophic stage.

174 nal activity and protein accumulation at the necrotrophic stage.

175 or enhanced JA-dependent defenses during the necrotrophic stages of infection.

176 mechanism includes sequential biotrophic and necrotrophic stages.

177 ic vs. non-pathogenic) and pathogenic niche (necrotrophic vs. biotrophic).