The Pseudomonas syringae type III effector HopG1 targets mitochondria, alters plant development and suppresses plant innate immunity
Article first published online: 27 OCT 2009
© 2009 Blackwell Publishing Ltd
Volume 12, Issue 3, pages 318–330, March 2010
How to Cite
Block, A., Guo, M., Li, G., Elowsky, C., Clemente, T. E. and Alfano, J. R. (2010), The Pseudomonas syringae type III effector HopG1 targets mitochondria, alters plant development and suppresses plant innate immunity. Cellular Microbiology, 12: 318–330. doi: 10.1111/j.1462-5822.2009.01396.x
- Issue published online: 5 FEB 2010
- Article first published online: 27 OCT 2009
- Received 17 June, 2009; revised 25 September, 2009; accepted 10 October, 2009.
The bacterial plant pathogen Pseudomonas syringae uses a type III protein secretion system to inject type III effectors into plant cells. Primary targets of these effectors appear to be effector-triggered immunity (ETI) and pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI). The type III effector HopG1 is a suppressor of ETI that is broadly conserved in bacterial plant pathogens. Here we show that HopG1 from P. syringae pv. tomato DC3000 also suppresses PTI. Interestingly, HopG1 localizes to plant mitochondria, suggesting that its suppression of innate immunity may be linked to a perturbation of mitochondrial function. While HopG1 possesses no obvious mitochondrial signal peptide, its N-terminal two-thirds was sufficient for mitochondrial localization. A HopG1–GFP fusion lacking HopG1's N-terminal 13 amino acids was not localized to the mitochondria reflecting the importance of the N-terminus for targeting. Constitutive expression of HopG1 in Arabidopsis thaliana, Nicotiana tabacum (tobacco) and Lycopersicon esculentum (tomato) dramatically alters plant development resulting in dwarfism, increased branching and infertility. Constitutive expression of HopG1 in planta leads to reduced respiration rates and an increased basal level of reactive oxygen species. These findings suggest that HopG1's target is mitochondrial and that effector/target interaction promotes disease by disrupting mitochondrial functions.