Soybean rust(SBR),caused by an obligate biotrophic pathogen Phakopsora pachyrhizi,is a devastating disease of soybean worldwide.However,the mechanisms underlying plant invasion by P.pachyrhizi are poorly understood,wh...Soybean rust(SBR),caused by an obligate biotrophic pathogen Phakopsora pachyrhizi,is a devastating disease of soybean worldwide.However,the mechanisms underlying plant invasion by P.pachyrhizi are poorly understood,which hinders the development of effective control strategies for SBR.Here we performed detailed histological characterization on the infection cycle of P.pachyrhizi in soybean and conducted a high-resolution transcriptional dissection of P.pachyrhizi during infection.This revealed P.pachyrhizi infection leads to significant changes in gene expression with 10 co-expressed gene modules,representing dramatic transcriptional shifts in metabolism and signal transduction during different stages throughout the infection cycle.Numerous genes encoding secreted protein are biphasic expressed,and are capable of inhibiting programmed cell death triggered by microbial effectors.Notably,three co-expressed P.pachyrhizi apoplastic effectors(PpAE1,PpAE2,and PpAE3) were found to suppress plant immune responses and were essential for P.pachyrhizi infection.Double-stranded RNA coupled with nanomaterials significantly inhibited SBR infection by targeting PpAE1,PpAE2,and PpAE3,and provided long-lasting protection to soybean against P.pachyrhizi.Together,this study revealed prominent changes in gene expression associated with SBR and identified P.pachyrhizi virulence effectors as promising targets of RNA interference-based soybean protection strategy against SBR.展开更多
The plant hormones salicylic acid(SA)and jasmonic acid(JA)act in mutual negative-feedback regulation to balance plant growth-defense trade-off.Heterotrimeric Gα-Gβ-Gγproteins are hubs that regulate defense signalin...The plant hormones salicylic acid(SA)and jasmonic acid(JA)act in mutual negative-feedback regulation to balance plant growth-defense trade-off.Heterotrimeric Gα-Gβ-Gγproteins are hubs that regulate defense signaling.In Arabidopsis,the Gα(GPA1)and Gβ(AGB1)subunits are required for defense against biotrophic and necrotrophic pathogens;however,the upstream and downstream molecular mechanisms underlying G protein-mediated defense remain largely unclear.In this study,we found that G proteins are primarily negative regulators of JA signaling in response to pathogen attack.Both TCP14 and JAZs are transcriptional regulators in the JA pathways.We revealed that GPA1 interacts with TCP14 within nuclear foci,and AGB1 interacts with TCP14 and most of JAZ regulators,including JAZ3.Mechanistically,GPA1 slows the proteasomal degradation of the G protein-TCP14-JAZ3 complex,a process that is normally promoted by JA and the bacterial virulence effector HopBB1,thus boosting SA-based defense.In turn,GPA1 activity is regulated by JA-induced phosphorylation at a conserved residue located near the nucleotide-binding pocket and other residues within the N-terminalαhelix.The phosphomimic mutations do not affect GTP binding or hydrolysis but enhance GPA1 interaction with TCP14 and JAZ3,thereby preventing their degradation.This newly discovered phosphorylation-dependent mechanism of de-sequestering G protein partners to modulate transcriptional regulation may extend to both yeast and human cells.展开更多
基金supported by grants from the National Key Research and Development Program of China(2022YFF1001500)the Fundamental Research Funds for the Central Universities(CGPY2024001)the Zhongshan Biological Breeding Laboratory(ZSBBL-KY2023-03)。
文摘Soybean rust(SBR),caused by an obligate biotrophic pathogen Phakopsora pachyrhizi,is a devastating disease of soybean worldwide.However,the mechanisms underlying plant invasion by P.pachyrhizi are poorly understood,which hinders the development of effective control strategies for SBR.Here we performed detailed histological characterization on the infection cycle of P.pachyrhizi in soybean and conducted a high-resolution transcriptional dissection of P.pachyrhizi during infection.This revealed P.pachyrhizi infection leads to significant changes in gene expression with 10 co-expressed gene modules,representing dramatic transcriptional shifts in metabolism and signal transduction during different stages throughout the infection cycle.Numerous genes encoding secreted protein are biphasic expressed,and are capable of inhibiting programmed cell death triggered by microbial effectors.Notably,three co-expressed P.pachyrhizi apoplastic effectors(PpAE1,PpAE2,and PpAE3) were found to suppress plant immune responses and were essential for P.pachyrhizi infection.Double-stranded RNA coupled with nanomaterials significantly inhibited SBR infection by targeting PpAE1,PpAE2,and PpAE3,and provided long-lasting protection to soybean against P.pachyrhizi.Together,this study revealed prominent changes in gene expression associated with SBR and identified P.pachyrhizi virulence effectors as promising targets of RNA interference-based soybean protection strategy against SBR.
基金supported by The Division of Chemical Sciences,Geosciences,and Biosciences,Office of Basic Energy Sciences of the US Department of Energy through grant DE-FG02-05er15671A.M.J.Funding was also provided by NIGMS(R01GM065989)and NSF(MCB-0718202 and IOS-2034929)awarded to A.M.J.,NIH grant(R35GM118105)awarded to H.G.D.,grant PID2021-1260060OB-I00 funded by MCIN/AEI/10.13039/501100011033by“ERDFAway of making Europe"to A.M.and L.J.
文摘The plant hormones salicylic acid(SA)and jasmonic acid(JA)act in mutual negative-feedback regulation to balance plant growth-defense trade-off.Heterotrimeric Gα-Gβ-Gγproteins are hubs that regulate defense signaling.In Arabidopsis,the Gα(GPA1)and Gβ(AGB1)subunits are required for defense against biotrophic and necrotrophic pathogens;however,the upstream and downstream molecular mechanisms underlying G protein-mediated defense remain largely unclear.In this study,we found that G proteins are primarily negative regulators of JA signaling in response to pathogen attack.Both TCP14 and JAZs are transcriptional regulators in the JA pathways.We revealed that GPA1 interacts with TCP14 within nuclear foci,and AGB1 interacts with TCP14 and most of JAZ regulators,including JAZ3.Mechanistically,GPA1 slows the proteasomal degradation of the G protein-TCP14-JAZ3 complex,a process that is normally promoted by JA and the bacterial virulence effector HopBB1,thus boosting SA-based defense.In turn,GPA1 activity is regulated by JA-induced phosphorylation at a conserved residue located near the nucleotide-binding pocket and other residues within the N-terminalαhelix.The phosphomimic mutations do not affect GTP binding or hydrolysis but enhance GPA1 interaction with TCP14 and JAZ3,thereby preventing their degradation.This newly discovered phosphorylation-dependent mechanism of de-sequestering G protein partners to modulate transcriptional regulation may extend to both yeast and human cells.
