Pyropia yezoensis , one of the most economically important marine algae, suffers from the biotic stress of oomycete necrotrophic pathogen Pythium porphyrae . However, little is known about the molecular defensive mechanisms employed by Pyr. yezoensis during the infection process. In the present study, we defined three stages of infection based on the histopathological features and photosynthetic physiology. Transcriptomic analysis was carried out at different stages of infection to identify the genes related to the innate immune system in Pyr. yezoensis . In total, 2139 up-regulated genes and 1672 down-regulated genes were identified from all the infected groups. Three upregulated genes encoding extracellular lectin domains (one C-type lectin gene and two L-type lectin genes) were predicted to be p attern r ecognition r eceptors (PRRs) that activate PAMP-triggered immunity (PTI). Several defense mechanisms that were typically regarded as PTI in plants were induced during the infection. These include defensive and protective enzymes, heat shock proteins, secondary metabolites, cellulase, and protease inhibitors. Twenty-three genes that encode typical plant R protein domains (LRR, NBS, or TIR) were found to be up-regulated after infection. They were likely to be regarded as candidates of putative R proteins in Pyr. yezoensis . As a part of E ffector-t riggered i mmunity (ETI), expression of genes related to the ubiquitin-proteasome system (UPS) and hypersensitive cell death response (HR) increased significantly during the infection. The current study suggests that, similar to plants, Pyr. yezoensis possesses a relatively complete innate immune system to counter the invasion of necrotrophic pathogen Pyt. porphyrae . However, innate immunity genes of Pyr. yezoensis appear to be more ancient in origin compared to that in plants.
BackgroundPlant suffer from a variety of diseases that are caused by fungi [1-3], oomycetes [4,5], bacteria [6] and viruses [7][8][9]. It is evident that plants rely on their innate immune system to resist infection by the pathogens. Jones proposed a four-phased 'zigzag' model to illustrate how the plants' innate immune system fights against the pathogen [10]. At the onset, the plant recognizes the pathogenassociated molecular patterns (PAMPs) by their transmembrane pattern recognition receptors (PRRs) to activate PAMP-triggered immunity (PTI). PTI includes callose deposition [11,12], cell-wall 3 thickening [13,14] and reactive oxygen species (ROS) production [15,16], to control the colonization of pathogen nonspecifically. Next, pathogen interferes with the PTI by its effectors, resulting in effector-triggered susceptibility (ETS) of the plant. Further, the plant specifically recognizes effectors via R proteins either directly or indirectly to activate ETI[17]. ETI can amplify PTI and enhance the resistance by activating the hypersensitive cell death in the plant. Finally, pathogen represses ETI by modifying or acquiring new effectors that prevent the recognition of R proteins, further induci...