Root-knot nematodes(RKNs)cause huge agricultural losses every year.They secrete a repertoire of effectors to facilitate parasitism through the induction of plant-derived giant feeding cells,which serve as their sole s...Root-knot nematodes(RKNs)cause huge agricultural losses every year.They secrete a repertoire of effectors to facilitate parasitism through the induction of plant-derived giant feeding cells,which serve as their sole source of nutrients.However,the mode of action of these effectors and their targeted host pro-teins remain largely unknown.In this study,we investigated the role of the effector Mi2G02 in Meloidogyne incognita parasitism.Host-derived Mi2G02 RNA interference in Arabidopsis thaliana affected giant cell development,whereas ectopic expression of Mi2G02 promoted root growth and increased plant sus-ceptibility to M.incognita.We used various combinations of approaches to study the specific interactions between Mi2G02 and A.thaliana GT-3a,a trihelix transcription factor.GT-3a knockout in A.thaliana affected feeding-site development,resulting in production of fewer egg masses,whereas GT-3a overex-pression in A.thaliana increased susceptibility to M.incognita and also root growth.Moreover,we demon-strated that Mi2G02 plays a role in maintaining GT-3a protein stabilization by inhibiting the 26S proteasome-dependent pathway,leading to suppression of TOZ and RAD23C expression and thus promoting nematode parasitism.This work enhances our understanding of how a pathogen effector manipulates the role and regulation of a transcription factor by interfering with a proteolysis pathway to reprogram gene expression for development of nematode feeding cells.展开更多
基金supported by the Youth Innovation Program of the Chinese Academy of Agricultural Sciences (grant no.Y2022QC06)the National Natural Science Foundation of China (grant nos.32001878,32172366)+2 种基金the Natural Science Foundation of Beijing (grant no.6222054)the China Agricultural Research System (CARS-23)the French Government (National Research Agency,ANR)through"Investments for the Future"LabEx SIGNALIFE (#ANR-11-LABX-0028-01),IDEX UCAJedi (#ANR-15-IDEX-0).
文摘Root-knot nematodes(RKNs)cause huge agricultural losses every year.They secrete a repertoire of effectors to facilitate parasitism through the induction of plant-derived giant feeding cells,which serve as their sole source of nutrients.However,the mode of action of these effectors and their targeted host pro-teins remain largely unknown.In this study,we investigated the role of the effector Mi2G02 in Meloidogyne incognita parasitism.Host-derived Mi2G02 RNA interference in Arabidopsis thaliana affected giant cell development,whereas ectopic expression of Mi2G02 promoted root growth and increased plant sus-ceptibility to M.incognita.We used various combinations of approaches to study the specific interactions between Mi2G02 and A.thaliana GT-3a,a trihelix transcription factor.GT-3a knockout in A.thaliana affected feeding-site development,resulting in production of fewer egg masses,whereas GT-3a overex-pression in A.thaliana increased susceptibility to M.incognita and also root growth.Moreover,we demon-strated that Mi2G02 plays a role in maintaining GT-3a protein stabilization by inhibiting the 26S proteasome-dependent pathway,leading to suppression of TOZ and RAD23C expression and thus promoting nematode parasitism.This work enhances our understanding of how a pathogen effector manipulates the role and regulation of a transcription factor by interfering with a proteolysis pathway to reprogram gene expression for development of nematode feeding cells.
