Abstract
The universal nature of networks’ structural and physical properties across diverse systems offers a better prospect to elucidate the interplay between a system and its environment. In the last decade, several large-scale transcriptome and interactome studies were conducted to understand the complex and dynamic nature of interactions between Arabidopsis and its bacterial pathogen, Pseudomonas syringae pv. tomato DC3000. We took advantage of these publicly available datasets and performed “-omics”-based integrative, and network topology analyses to decipher the transcriptional and protein-protein interaction activities of effector targets. We demonstrated that effector targets exhibit shorter distance to differentially expressed genes (DEGs) and possess increased information centrality. Intriguingly, effector targets are differentially expressed in a sequential manner and make for 1% of the total DEGs at any time point of infection with virulent or defense-inducing DC3000 strains. We revealed that DC3000 significantly alters the expression levels of 71% effector targets and their downstream physical interacting proteins in Arabidopsis interactome. Our integrative “-omics”-–based analyses identified dynamic complexes associated with MTI and disease susceptibility. Finally, we discovered five novel plant defense players using a systems biology-fueled top-to-bottom approach and demonstrated immune-related functions for them, further validating the power and resolution of our network analyses.
Highlights
While plants are exposed to a wide range of biotic and abiotic stresses, they possess a robust and resilient cellular architecture that allows them to adapt to constantly changing environments[1, 2]
To understand the dynamic transcriptional and protein-protein interaction behaviors of effector targets, we took advantage of high-resolution dynamic transcriptome data generated by Lewis et al.[29] as well as interactome data extracted from AI-1MAIN, PPIN-1, and PPIN-2, and performed additional network biology analyses
Given that effector targets exhibit an increased degree compared to non targets[31,32,33], we hypothesized that diverse pathogens interact with effector targets to interfere with the flow of information
Summary
While plants are exposed to a wide range of biotic and abiotic stresses, they possess a robust and resilient cellular architecture that allows them to adapt to constantly changing environments[1, 2]. In addition to PRRs, plants have evolved another class of sensors known as nucleotide binding-LRR (NLR) receptors These NLRs can directly perceive pathogen virulence molecules (hereafter called effectors) or monitor the activities of effectors on host proteins (indirect recognition) and initiate a defense response termed effector-triggered immunity (ETI)[17,18,19,20,21]. The activation of these defenses involves massive spatiotemporal transcriptional reprogramming involving intricate signal transduction pathways through largely unknown mechanisms[22, 24, 25] Specialized pathogens such as the bacterial pathogen Pseudomonas syringae secrete and deliver effectors into the plant cells[26] using type three secretion system (TTSS). Our dynamic subnetwork analysis identified novel five key proteins involved in plant immunity
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