2024-03-28T23:36:42Zhttp://digital.csic.es/dspace-oai/requestoai:digital.csic.es:10261/1528572021-12-28T16:45:17Zcom_10261_122com_10261_6col_10261_375
00925njm 22002777a 4500
dc
Rufián, José S.
author
Lucía, Ainhoa
author
Macho, Alberto P.
author
Orozco-Navarrete, Begoña
author
Arroyo-Mateos, Manuel
author
Bejarano, Eduardo R.
author
Beuzón, Carmen R.
author
Ruiz-Albert, Javier
author
2015-07-08
The Pseudomonas syringae type III-secreted effector HopZ1a is a member of the HopZ/YopJ superfamily of effectors that triggers immunity in Arabidopsis. We have previously shown that HopZ1a suppresses both local [effector-triggered immunity (ETI)] and systemic immunity [systemic acquired resistance (SAR)] triggered by the heterologous effector AvrRpt2. HopZ1a has been shown to possess acetyltransferase activity, and this activity is essential to trigger immunity in Arabidopsis. HopZ1a acetyltransferase activity has been reported to require the auto-acetylation of the effector on a specific lysine (K289) residue. In this paper we analyze the relevance of autoacetylation of lysine residue 289 in HopZ1a ability to suppress plant defenses, and on the light of the results obtained, we also revise its relevance for HopZ1a avirulence activity. Our results indicate that, while the HopZ1aK289R mutant is impaired to some degree in its virulence and avirulence activities, is by no means phenotypically equivalent to the catalytically inactive HopZ1aC216A, since it is still able to trigger a defense response that induces detectable macroscopic HR and effectively protects Arabidopsis from infection, reducing growth of P. syringae within the plant. We also present evidence that the HopZ1aK289R mutant still displays virulence activities, partially suppressing both ETI and SAR.
Frontiers in Microbiology 6: 684 (2015)
1664-302X
http://hdl.handle.net/10261/152857
10.3389/fmicb.2015.00684
http://dx.doi.org/10.13039/501100000780
http://dx.doi.org/10.13039/501100003329
http://dx.doi.org/10.13039/501100004837
http://dx.doi.org/10.13039/501100011011
26217317
Auto-acetylation on K289 is not essential for HopZ1a-mediated plant defense suppression