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--- bacteria:t3e:xopj2 [2020/08/09 13:00]
bosis
+++ bacteria:t3e:xopj2 [2020/08/11 14:43] (current)
rkoebnik
@@ Line 2: / Line 2: @@
 Author: [[https://www.researchgate.net/profile/Daiva_Burokiene|Daiva Burokienė]]\\
-Internal reviewer: Eran Bosis\\
+Internal reviewer: [[https://www.researchgate.net/profile/Eran_Bosis|Eran Bosis]]\\
 Expert reviewer: FIXME
@@ Line 32: / Line 32: @@
   * Resistance in Pi-0 was found to be caused by a recessive mutation predicted to inactivate a carboxylesterase known to hydrolyze lysophospholipids and acylated proteins in eukaryotes. Transgenic Pi-0 plants expressing the wild-type allele from the //A. thaliana//  ecotype Columbia were susceptible to //Pst//  DC3000 AvrRpt2-AvrBsT-HA infection. These data indicated that the carboxylesterase inhibits AvrBsT-triggered phenotypes in //Arabidopsis//, and the resistance gene was therefore called //SOBER1//  (Suppressor Of AvrBsT-Elicited Resistance 1), where the inactive allele in Pi-0, //sober1-1//, provides resistance (Cunnac //et al//., 2007).
   * It was later shown that Pi-0 leaves infected with //Pst//  DC3000 expressing AvrBsT accumulated higher levels of phosphatidic acid (PA) compared to leaves infected with //Pst//  DC3000. Phospholipase D (PLD) activity was required for high PA levels and AvrBsT-dependent HR in Pi-0. Overexpression of SOBER1 in Pi-0 reduced PA levels and inhibited HR. These data implicated PA, phosphatidylcholine (PC) and lysophosphatidylcholine (LysoPC) as potential SOBER1 substrates. Recombinant His<sub>6</sub>-SOBER1 hydrolyzed PC but not PA or LysoPC in vitro indicating that the enzyme has phospholipase A2 (PLA2) activity. Chemical inhibition of PLA2 activity in leaves expressing SOBER1 resulted in HR in response to Pst DC3000 AvrBsT. These data were consistent with the model that SOBER1 PLA2 activity suppresses PLD-dependent production of PA in response to AvrBsT elicitation (Kirik //et al//., 2009).
-  * Transgenic //Arabidopsis//  plants overexpression AvrBsT upon dexamethasone (DEX) induction showed reduced susceptibility to infection with the obligate biotrophic oomycete //Hyaloperonospora arabidopsidis//  (Hwang //et al//., 2012). In contrast, plants overexpressing dexamethasone //(DEX)//://avrBsT// exhibited enhanced susceptibility to //Pseudomonas syringae//  pv. //tomato//  (Pst) DC3000 infection (Hwang //et al//., 2012). Thus, AvrBsT overexpression leads to both disease and defense responses to microbial pathogens of different lifestyles (Hwang //et al//., 2012).
+  * Transgenic //Arabidopsis//  plants overexpression AvrBsT upon dexamethasone (DEX) induction showed reduced susceptibility to infection with the obligate biotrophic oomycete //Hyaloperonospora arabidopsidis//  (Hwang //et al//., 2012). In contrast, plants overexpressing dexamethasone //(DEX)//://avrBsT//  exhibited enhanced susceptibility to //Pseudomonas syringae//  pv. //tomato//  (Pst) DC3000 infection (Hwang //et al//., 2012). Thus, AvrBsT overexpression leads to both disease and defense responses to microbial pathogens of different lifestyles (Hwang //et al//., 2012).
   * Phylogenomics revealed that a host-range expansion of //X. euvesicatoria//  pv. //perforans//  (//Xep//) field strains on pepper is due, in part, to a loss of the effector AvrBsT. Further studies with //Xep//  demonstrated that a double deletion of //avrBsT//  and //xopQ//  allowed a host range expansion for //Nicotiana benthamiana//  (Schwartz //et al//., 2015).
   * Later, AvrBsT was found to contribute to fitness of //Xep//  on tomato plants under field conditions (Abrahamian //et al//., 2018).

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