Plants utilize nucleotide-binding,leucine-rich repeat receptors(NLRs)to detect pathogen effectors,leading to effector-triggered immunity.The NLR ZAR1 indirectly recognizes the Xanthomonas campestris pv.campestris effe...Plants utilize nucleotide-binding,leucine-rich repeat receptors(NLRs)to detect pathogen effectors,leading to effector-triggered immunity.The NLR ZAR1 indirectly recognizes the Xanthomonas campestris pv.campestris effector AvrAC and Pseudomonas syringae effector HopZIa by associating with closely related receptor-like cytoplasmic kinase subfamily XII-2(RLCK XII-2)members RKS1 and ZED1,respectively.ZAR1,RKS1,and the AvrAC-modified decoy PBL2ump form a pentameric resistosome in vitro,and the ability of resistosome formation is required for AvrAC-triggered cell death and disease resistance.However,it remains unknown whether the effectors induce ZAR1 oligomerization in the plant cell.In this study,we show that both AvrAC and HopZ1 a can induce oligomerization of ZAR1 in Arabidopsis protoplasts.Residues mediating ZAR1-ZED1 interaction are indispensable for HopZIa-induced ZAR1 oligomerization in vivo and disease resistance.In addition,ZAR1 residues required for the assembly of ZAR1 resistosome in vitro are also essential for HopZIa-induced ZAR1 oligomerization in vivo and disease resistance.Our study provides evidence that pathogen effectors induce ZAR1 resistosome formation in the plant cell and that the resistosome formation triggers disease resistance.展开更多
Pseudomonas syringae pv.actinidiae(Psa)causes bacterial canker,a devastating disease threatening the Actinidia fruit industry.In a search for non-host resistance genes against Psa,we find that the nucleotidebinding le...Pseudomonas syringae pv.actinidiae(Psa)causes bacterial canker,a devastating disease threatening the Actinidia fruit industry.In a search for non-host resistance genes against Psa,we find that the nucleotidebinding leucine-rich repeat receptor(NLR)protein ZAR1 from both Arabidopsis and Nicotiana benthamiana(Nb)recognizes Hop Z5 and triggers cell death.The recognition requires ZED1 in Arabidopsis and JIM2 in Nb plants,which are members of the ZRK pseudokinases and known components of the ZAR1 resistosome.Surprisingly,Arabidopsis ZAR1 and RPM1,another NLR known to recognize Hop Z5,confer disease resistance to Hop Z5 in a strain-specific manner.Thus,ZAR1,but not RPM1,is solely required for resistance to P.s.maculicola ES4326(Psm)carrying hop Z5,whereas RPM1 is primarily required for resistance to P.s.tomato DC3000(Pst)carrying hop Z5.Furthermore,the ZAR1-mediated resistance to Psm hop Z5 in Arabidopsis is insensitive to SOBER1,which encodes a deacetylase known to suppress the RPM1-mediated resistance to Pst hop Z5.In addition,hop Z5 enhances P.syringae virulence in the absence of ZAR1 or RPM1 and that SOBER1 abolishes such virulence function.Together the study suggests that ZAR1 may be used for improving Psa resistance in Actinidia and uncovers previously unknown complexity of effectortriggered immunity and effector-triggered virulence.展开更多
Poor oocyte quality is associated with early embryo developmental arrest and infertility.Maternal gene plays crucial roles in the regulation of oocyte maturation,and its mutation is a common cause of female infertilit...Poor oocyte quality is associated with early embryo developmental arrest and infertility.Maternal gene plays crucial roles in the regulation of oocyte maturation,and its mutation is a common cause of female infertility.However,how to improve oocyte quality and develop effective therapy for maternal gene mutation remains elusive.Here,we use Zar1 as an example to assess the feasibility of genome transfer to cure maternal gene mutationecaused female infertility.We first discover that cytoplasmic deficiency primarily leads to Zar1-null embryo developmental arrest by disturbing maternal transcript degradation and minor zygotic genome activation(ZGA)during the maternal-zygotic transition.We next perform genome transfer at the oocyte(spindle transfer or polar body transfer)and zygote(early pronuclear transfer or late pronuclear transfer)stages to validate the feasibility of preventing Zar1 mutationecaused infertility.We finally demonstrate that genome transfer either at the oocyte or at the early pronuclear stage can support normal preimplantation embryo development and produce live offspring.Moreover,those pups grow to adulthood and show normal fertility.Therefore,our findings provide an effective basis of therapies for the treatment of female infertility caused by maternal gene mutation.展开更多
Plants utilize intracellular nucleotide-binding leucine-rich repeat domain-containing receptors (NLRs) to recognize pathogen effectors and induce a robust defense response named effector-triggered immunity (ETI). The ...Plants utilize intracellular nucleotide-binding leucine-rich repeat domain-containing receptors (NLRs) to recognize pathogen effectors and induce a robust defense response named effector-triggered immunity (ETI). The Arabidopsis NLR protein HOPZ-ACTIVATED RESISTANCE 1 (ZAR1) forms a precomplex with HOPZ-ETI-DEFICIENT 1 (ZED1),a receptor-like cytoplasmic kinase (RLCK) XII-2 subfamily member, to recognize the Pseudomonas syringae effector HopZ1 a. We previously described a dominant mutant of Arabi-dopsis ZED1, zed1-D, which displays temperature-sensitive autoimmunity in a ZAR1-dependent manner. Here, we report that the RLCKs SUPPRESSOR OF ZED1-D1 (SZE1) and SZE2 associate with the ZAR1-ZED1 complex and are required for the ZED7-D-activated autoimmune response and HopZ1a-triggered immunity. We show that SZE1 but not SZE2 has autophosphorylation activity, and that the N-terminal myristoylation of both SZE1 and SZE2 is critical for their plasma membrane localization and ZED1-D-activated autoimmunity. Furthermore, we demonstrate that SZE1 and SZE2 both interact with ZAR1 to form ja functional complex and are required for resistance against P. syringae pv. tomato DC3000 ex-pressing HopZIa. We also provide evidence that SZE1 and SZE2 interact with HopZ1a and function together with ZED1 to change the intramolecular interactions of ZAR1, leading to its activation. Taken together, our re-sults reveal SZE1 and SZE2 as critical signaling components of HopZ1a-triggered immunity.展开更多
基金grants from National Natural Science Foundation of China(31521001)Ministry of Science and Technology of the People's Republic of China(2016YFD0100601)the Chinese Academy of Sciences international cooperation key project grant GJHZ1311,and the State Key Laboratory of Plant Genomics(SKLPG2016B-2)to J.-M.Z.
文摘Plants utilize nucleotide-binding,leucine-rich repeat receptors(NLRs)to detect pathogen effectors,leading to effector-triggered immunity.The NLR ZAR1 indirectly recognizes the Xanthomonas campestris pv.campestris effector AvrAC and Pseudomonas syringae effector HopZIa by associating with closely related receptor-like cytoplasmic kinase subfamily XII-2(RLCK XII-2)members RKS1 and ZED1,respectively.ZAR1,RKS1,and the AvrAC-modified decoy PBL2ump form a pentameric resistosome in vitro,and the ability of resistosome formation is required for AvrAC-triggered cell death and disease resistance.However,it remains unknown whether the effectors induce ZAR1 oligomerization in the plant cell.In this study,we show that both AvrAC and HopZ1 a can induce oligomerization of ZAR1 in Arabidopsis protoplasts.Residues mediating ZAR1-ZED1 interaction are indispensable for HopZIa-induced ZAR1 oligomerization in vivo and disease resistance.In addition,ZAR1 residues required for the assembly of ZAR1 resistosome in vitro are also essential for HopZIa-induced ZAR1 oligomerization in vivo and disease resistance.Our study provides evidence that pathogen effectors induce ZAR1 resistosome formation in the plant cell and that the resistosome formation triggers disease resistance.
基金supported by grants from the National Key R&D Program of China (2021YFA1300701) to J.M.Z.the National Natural Science Foundation of China (31872654) to Z.Y.Z.the Hainan Excellent Talent Team, and the State Key Laboratory of Plant Genomics (SKLPG2016B-2) to J.M.Z
文摘Pseudomonas syringae pv.actinidiae(Psa)causes bacterial canker,a devastating disease threatening the Actinidia fruit industry.In a search for non-host resistance genes against Psa,we find that the nucleotidebinding leucine-rich repeat receptor(NLR)protein ZAR1 from both Arabidopsis and Nicotiana benthamiana(Nb)recognizes Hop Z5 and triggers cell death.The recognition requires ZED1 in Arabidopsis and JIM2 in Nb plants,which are members of the ZRK pseudokinases and known components of the ZAR1 resistosome.Surprisingly,Arabidopsis ZAR1 and RPM1,another NLR known to recognize Hop Z5,confer disease resistance to Hop Z5 in a strain-specific manner.Thus,ZAR1,but not RPM1,is solely required for resistance to P.s.maculicola ES4326(Psm)carrying hop Z5,whereas RPM1 is primarily required for resistance to P.s.tomato DC3000(Pst)carrying hop Z5.Furthermore,the ZAR1-mediated resistance to Psm hop Z5 in Arabidopsis is insensitive to SOBER1,which encodes a deacetylase known to suppress the RPM1-mediated resistance to Pst hop Z5.In addition,hop Z5 enhances P.syringae virulence in the absence of ZAR1 or RPM1 and that SOBER1 abolishes such virulence function.Together the study suggests that ZAR1 may be used for improving Psa resistance in Actinidia and uncovers previously unknown complexity of effectortriggered immunity and effector-triggered virulence.
基金primarily supported by the Ministry of Science and Technology of the People’s Republic of China(2017YFA0102602,2016YFA0100400)supported by the National Natural Science Foundation of China(81630035,31871448,31721003)+3 种基金the Shanghai Subject Chief Scientist Program(15XD1503500)Supporting Project of Medical Guidance(Western Medicine)of Science and Technology Commission of Shanghai Municipality(15411964600)Merck Serono China Research Fund for Fertility Experts,the Shanghai municipal medical and health discipline construction projects(2017ZZ02015)the Fundamental Research Funds for the Central Universities(1515219049)。
文摘Poor oocyte quality is associated with early embryo developmental arrest and infertility.Maternal gene plays crucial roles in the regulation of oocyte maturation,and its mutation is a common cause of female infertility.However,how to improve oocyte quality and develop effective therapy for maternal gene mutation remains elusive.Here,we use Zar1 as an example to assess the feasibility of genome transfer to cure maternal gene mutationecaused female infertility.We first discover that cytoplasmic deficiency primarily leads to Zar1-null embryo developmental arrest by disturbing maternal transcript degradation and minor zygotic genome activation(ZGA)during the maternal-zygotic transition.We next perform genome transfer at the oocyte(spindle transfer or polar body transfer)and zygote(early pronuclear transfer or late pronuclear transfer)stages to validate the feasibility of preventing Zar1 mutationecaused infertility.We finally demonstrate that genome transfer either at the oocyte or at the early pronuclear stage can support normal preimplantation embryo development and produce live offspring.Moreover,those pups grow to adulthood and show normal fertility.Therefore,our findings provide an effective basis of therapies for the treatment of female infertility caused by maternal gene mutation.
基金National Natural Science Foundation of China (31471160)the Strategic Priority Research Program of Chinese Academy of Sciences PCDB27030102).
文摘Plants utilize intracellular nucleotide-binding leucine-rich repeat domain-containing receptors (NLRs) to recognize pathogen effectors and induce a robust defense response named effector-triggered immunity (ETI). The Arabidopsis NLR protein HOPZ-ACTIVATED RESISTANCE 1 (ZAR1) forms a precomplex with HOPZ-ETI-DEFICIENT 1 (ZED1),a receptor-like cytoplasmic kinase (RLCK) XII-2 subfamily member, to recognize the Pseudomonas syringae effector HopZ1 a. We previously described a dominant mutant of Arabi-dopsis ZED1, zed1-D, which displays temperature-sensitive autoimmunity in a ZAR1-dependent manner. Here, we report that the RLCKs SUPPRESSOR OF ZED1-D1 (SZE1) and SZE2 associate with the ZAR1-ZED1 complex and are required for the ZED7-D-activated autoimmune response and HopZ1a-triggered immunity. We show that SZE1 but not SZE2 has autophosphorylation activity, and that the N-terminal myristoylation of both SZE1 and SZE2 is critical for their plasma membrane localization and ZED1-D-activated autoimmunity. Furthermore, we demonstrate that SZE1 and SZE2 both interact with ZAR1 to form ja functional complex and are required for resistance against P. syringae pv. tomato DC3000 ex-pressing HopZIa. We also provide evidence that SZE1 and SZE2 interact with HopZ1a and function together with ZED1 to change the intramolecular interactions of ZAR1, leading to its activation. Taken together, our re-sults reveal SZE1 and SZE2 as critical signaling components of HopZ1a-triggered immunity.
