Oxidative burst and cognate redox signalling reported by luciferase imaging: identification of a signal network that functions independently of ethylene, SA and Me-JA but is dependent on MAPKK activity
Jj. Grant et al., Oxidative burst and cognate redox signalling reported by luciferase imaging: identification of a signal network that functions independently of ethylene, SA and Me-JA but is dependent on MAPKK activity, PLANT J, 24(5), 2000, pp. 569-582
Recognition of avirulent microbial pathogens activates an oxidative burst l
eading to the accumulation of reactive oxygen intermediates (ROIs), which a
re thought to integrate a diverse set of defence mechanisms resulting in th
e establishment of plant disease resistance. A novel transgenic Arabidopsis
line containing a gst1::luc transgene was developed and employed to report
the temporal and spatial dynamics of ROI accumulation and cognate redox si
gnalling in response to attempted infection by avirulent strains of Pseudom
onas syringae pv. tomato (Pst). Strong engagement of the oxidative burst wa
s dependent on the presence of functional Pst hrpS and hrpA gene products.
Experiments employing pharmacological agents suggested that at least two di
stinct sources, including an NADPH oxidase and a peroxidase-type enzyme, co
ntributed to the generation of redox cues. The analysis of gst1 and pall ge
ne expression in nahG, coi1 and etr1 plants suggested that engagement of th
e oxidative burst and cognate redox signalling functioned independently of
salicylic acid, methyl jasmonate and ethylene. in contrast, studies using a
panel of protein kinase and phosphatase inhibitors and in-gel kinase assay
s in these mutant backgrounds suggested that a 48 kDa mitogen-activated pro
tein kinase (MAPK) activity was required for the activation of gst1 and pal
1 in response to redox cues. Thus the engagement of a bifurcating redox sig
nalling pathway possessing a MAPK module may contribute both to the establi
shment of plant disease resistance, and to the development of cellular prot
ectant mechanisms.