Manipulation of host S-nitrosylation by Pseudomonas syringae
Saidi, Noor Baity
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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.