Open Access
RNAi of the sesquiterpene cyclase gene for phytoalexin production impairs pre‐ and post‐invasive resistance to potato blight pathogens
Author(s) -
Yoshioka Miki,
Adachi Ayako,
Sato Yutaka,
Doke Noriyuki,
Kondo Tatsuhiko,
Yoshioka Hirofumi
Publication year - 2019
Publication title -
molecular plant pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.945
H-Index - 103
eISSN - 1364-3703
pISSN - 1464-6722
DOI - 10.1111/mpp.12802
Subject(s) - phytophthora infestans , phytoalexin , biology , blight , pathogen , microbiology and biotechnology , transgene , alternaria solani , sesquiterpene , genetically modified crops , botany , gene , biochemistry , resveratrol
Summary Potato antimicrobial sesquiterpenoid phytoalexins lubimin and rishitin have been implicated in resistance to the late blight pathogen, Phytophthora infestans and early blight pathogen, Alternaria solani . We generated transgenic potato plants in which sesquiterpene cyclase, a key enzyme for production of lubimin and rishitin, is compromised by RNAi to investigate the role of phytoalexins in potato defence. The transgenic tubers were deficient in phytoalexins and exhibited reduced post‐invasive resistance to an avirulent isolate of P. infestans , resulting in successful infection of the first attacked cells without induction of cell death. However, cell death was observed in the subsequently penetrated cells. Although we failed to detect phytoalexins and antifungal activity in the extract from wild‐type leaves, post‐invasive resistance to avirulent P. infestans was reduced in transgenic leaves. On the other hand, A. solani frequently penetrated epidermal cells of transgenic leaves and caused severe disease symptoms presumably from a deficiency in unidentified antifungal compounds. The contribution of antimicrobial components to resistance to penetration and later colonization may vary depending on the pathogen species, suggesting that sesquiterpene cyclase‐mediated compounds participate in pre‐invasive resistance to necrotrophic pathogen A. solani and post‐invasive resistance to hemibiotrophic pathogen P. infestans .