Abstract
Many plant pathogens secrete virulence effectors into host cells to target important proteins in host cellular network. However, the dynamic interactions between effectors and host cellular network have not been fully understood. Here, an integrative network analysis was conducted by combining Arabidopsis thaliana protein–protein interaction network, known targets of Pseudomonas syringae and Hyaloperonospora arabidopsidis effectors, and gene expression profiles in the immune response. In particular, we focused on the characteristic network topology of the effector targets and differentially expressed genes (DEGs). We found that effectors tended to manipulate key network positions with higher betweenness centrality. The effector targets, especially those that are common targets of an individual effector, tended to be clustered together in the network. Moreover, the distances between the effector targets and DEGs increased over time during infection. In line with this observation, pathogen-susceptible mutants tended to have more DEGs surrounding the effector targets compared with resistant mutants. Our results suggest a common plant–pathogen interaction pattern at the cellular network level, where pathogens employ potent local impact mode to interfere with key positions in the host network, and plant organizes an in-depth defense by sequentially activating genes distal to the effector targets.
Highlights
Plants are under constant threat of a wide spectrum of pathogens including bacteria, oomycetes and fungi in the wild (Tsuda and Somssich, 2015)
We collected Arabidopsis-Pseudomonas syringae (Psy) and Hyaloperonospora arabidopsidis (Hpa) protein–protein interaction (PPI) from a previous publication (Mukhtar et al, 2011) and mapped them onto the comprehensive Arabidopsis PPI network, in which the proteins interacting with the effectors were tagged as the effector targets
52 Arabidopsis proteins interacting with 27 Psy effectors and 109 Arabidopsis proteins interacting with 52 Hpa effectors were obtained, in which 17 Arabidopsis proteins were targeted by the effectors from both pathogens
Summary
Plants are under constant threat of a wide spectrum of pathogens including bacteria, oomycetes and fungi in the wild (Tsuda and Somssich, 2015). Plants have evolved complicated immune systems against pathogens. Pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) and effector-triggered immunity (ETI) are two major phases of plant immunity (Thomma et al, 2011). Plants sense pathogens’ conserved PAMPs (e.g., flagellin) to trigger PTI. To subvert PTI, pathogens secrete a battery of effector proteins, which usually carry various enzymatic activities or enzyme inhibitor activities, to interfere with plant immunity (Dodds and Rathjen, 2010). Potent ETI can be activated on the recognition of these effectors by nucleotide binding-leucine rich repeat (NB-LRR) proteins, either directly (i.e., by interacting with the effectors directly) or indirectly (i.e., by interacting with the proteins attacked by the effectors) (Ye and Ting, 2008; Li and Zhang, 2016)
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