Abstract:[Background] Elicitin is small molecule compound secreted by the Oomycetes Phytophthora and Pythium that can induce immune response in the host. [Objective] Identify the elicitin gene family of Pythium porphyrae and analyze its structural features and possible mechanisms of action during the infection. [Methods] Screening the genome of Pythium porphyrae NBRC33253 for members of elicitin gene family using homologous alignment method. Analysis of the physicochemical properties and phylogeny of elicitin family using bioinformatics tools, combined with transcriptomic data and GO functional annotation to discuss possible mechanism of action during the infection. [Results] Twenty-two elicitin gene family members were identified in the Pythium porphyrae genome. 17 elicitin genes were extracellular secretory proteins, four were localized at the plasma membrane and one was anchored to the Golgi apparatus. The elicitin genes are simple and conserved in structure, containing 1-2 CDS sequences, with the number of amino acids ranging from 114 to 2 100 aa and the isoelectric point ranging from 3.61 to 9.88. The phylogenetic analysis revealed an expansion of elicitin family in Pythium porphyrae NBRC33253. Expression analysis showed that six elicitin genes was up-regulated and seven elicitin genes down-regulated after infection, indicating Pythium porphyrae elicitin gene presumably possessed multiple biological functions. As annotated by GO function to cellulose binding elicitor lectin (CBEL) and modulation by symbiont of host defense-related programmed cell death. [Conclusion] The elicitin gene family of Pythium porphyrae is structurally conserved and belongs to the ELL (elicitin-like) subfamily. Due to the annotation, elicitins in NBRC33253 showed several kinds of function, including cellulose binding excitor lectin (CBEL) which could accelerate programmed cell death in host cells by binding cellulose, attaching to the host surface, performing protein kinase activity, triggering host MAPK signaling pathway-mediated immune responses, and promoting HR cell death. This study provides theoretical basis for further elucidation of the pathogenic mechanism of Phythium porphyrae and genetic breeding for disease resistance traits in Pyropia.
