Open AccessThe Ralstonia solanacearum effector RipAK suppresses plant hypersensitive response by inhibiting the activity of host catalases
Author(s) -
Sun Yunhao,
Li Pai,
Deng Mengying,
Shen Dong,
Dai Guangyi,
Yao Nan,
Lu Yongjun
Publication year - 2017
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/cmi.12736
Subject(s) - biology , ralstonia solanacearum , effector , microbiology and biotechnology , heterologous , hypersensitive response , mutant , secretion , wild type , pathogen , type three secretion system , gene , biochemistry , plant disease resistance
Summary The destructive bacterial pathogen Ralstonia solanacearum delivers effector proteins via a type‐III secretion system for its pathogenesis of plant hosts. However, the biochemical functions of most of these effectors remain unclear. RipAK of R. solanacearum GMI1000 is a type‐III effector with unknown functions. Functional analysis demonstrated that in tobacco leaves, ripAK knockout bacteria produced an obvious hypersensitive response; also, infected tissues accumulated reactive oxygen species in a shorter period postinfection, compared with wild type. This strongly indicates that RipAK can inhibit hypersensitive response during infection. Further analysis showed that RipAK localizes to peroxisomes and interacts with host catalases (CATs) in plant cells. Truncation of 2 putative domains of RipAK caused it to fail to target the peroxisome and fail to interact with AtCATs, suggesting that RipAK localization depends on its interaction with CATs. Furthermore, heterologous expression of RipAK inhibited CAT activity in vivo and in vitro. Finally, compared with the ripAK mutant, infection with a bacterial strain overexpressing RipAK inhibited the transcription of many immunity‐associated genes in infected tobacco leaves at 2‐ and 4‐hr postinfection, although mRNA levels of NtCAT1 were upregulated. These data indicate that GMI1000 suppresses hypersensitive response by inhibiting host CATs through RipAK at early stages of infection.