Manipulation of host S-nitrosylation by Pseudomonas syringae
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Date
27/06/2011Author
Saidi, Noor Baity
Metadata
Abstract
Nitric oxide (NO) and S-nitrosothiols (SNOs) are widespread signalling molecules that
regulate immunity in animals and plants (Wendehenne et al., 2001). Previously, we have
reported that Arabidopsis thaliana S-nitrosoglutathione reductase, (AtGSNOR1) modulates
the extent of total cellular SNO formation, which subsequently regulates multiple modes of
plant disease resistance (Feechan et al., 2005). Loss-of-function mutations in AtGSNOR1,
leading to increased SNO levels, have recently been shown to result in S-nitrosylation of the
key defence regulators NPR1 and AtSABP3, blunting their activity and subsequently leading
to increased pathogen susceptibility (Tada et al., 2008; Wang et al., 2009). Thus, inhibiting
AtGSNOR1 function leading to increased SNOs, would potentially provide a good strategy
for bacterial effector proteins, delivered by the type III secretion system (TTSS), to promote
infection.
AtGSNOR1 is constitutively expressed in all organs in Arabidopsis and its expression is
induced by wounding stress avirulent and non-host pathogen. Using gas phase
chemiluminescence, we show that infection with Pseudomonas syringae pv. tomato strain
DC3000 (PstDC3000) resulted in increase SNO levels which is TTSS. At the same time,
RT-PCR and GUS analysis indicated that AtGSNOR1 expression was transiently suppressed
by PstDC3000 which is also TTSS-dependent. Therefore, PstDC3000 infection suppresses
denitrosylase function of AtGSNOR1 to increase SNO levels and this virulence effect is
delivered by at least one of the effector protein secreted through TTSS.
Several putative cis-acting elements were identified in AtGSNOR1 promoter through deletion
analysis including GT-box, W-box and MYB/MYC binding motif. These elements comprise
of positive and negative regulators which are critical for the induction and suppression of
AtGSNOR1 in response to pathogen infection.
A few transgenic plants expressing effector proteins were selected and tested for their
suppressive effect on AtGSNOR1 expression during PstDC3000 infection. HopAM1 effector
proteins showed the ability to suppress AtGSNOR1 when expressed in planta.