Phytophthora pathogens secrete a large arsenal of effectors that manipulate host processes to create an environment conducive to pathogen colonization. However, the underlying mechanisms by which Phytophthora effector...Phytophthora pathogens secrete a large arsenal of effectors that manipulate host processes to create an environment conducive to pathogen colonization. However, the underlying mechanisms by which Phytophthora effectors manipulate host plant cells still remain largely unclear. In this study, we report that PcAvr3a12, a Phytophthera capsici RXLR effector and a member of the Avr3a effector family, suppresses plant immunity by targeting and inhibiting host plant peptidyl-prolyl cis-trans isomerase （PPlase）. Overexpression of PcAvr3a 12 in Arabidopsis thaliana enhanced plant susceptibility to P. capsici. FKBP15-2, an endoplasmic reticulum （ER）-Iocalized protein, was identified as a host target of PcAvr3a12 during early P. capsici infection. Analyses of A. thaliana T-DNA insertion mutant （fkbp15-2）, RNAi, and overexpression lines consistently showed that FKBP15-2 positively regulates plant immunity in response to Phytophthora infection. FKBP15-2 possesses PPlase activity essential for its contribution to immunity but is directly suppressed by PcAvr3a12. Interestingly, we found that FKBP15-2 is involved in ER stress sensing and is required for ER stress-mediated plant immunity. Taken together, these results suggest that P. capsici deploys an RXLR effector, PcAvr3a12, to facilitate infection by targeting and suppressing a novel ER-Iocalized PPlase, FKBP15-2, which is required for ER stress-mediated plant immunity.展开更多
Phytophthora sojae Kanfman and Gerdemann （P. sojae） is one of the most prevalent pathogens and causes Phytophthora root rot, which limits soybean production worldwide. Development of resistant cultivars is a cost-ef...Phytophthora sojae Kanfman and Gerdemann （P. sojae） is one of the most prevalent pathogens and causes Phytophthora root rot, which limits soybean production worldwide. Development of resistant cultivars is a cost-effective approach to controlling this disease. In this study, 127 soybean germplasm were evaluated for their responses to Phytophthora sojae strain Pm28 using the hypocotyl inoculation technique, and 49 were found resistant to the strain. The hypocotyl of P1, P2, F1, and F2：3 of two crosses of Ludou 4 （resistant）×Youchu 4 （susceptible） and Cangdou 5 （resistant）×Williams （susceptible） were inoculated with Pm28, and were used to analyze the inheritance of resistance. The population derived from the cross of Ludou 4×Youchu 4 was used to map the resistance gene （designated as Rps9） to a linkage group. 932 pairs of SSR primers were used to detect polymorphism, and seven SSR markers were mapped near the resistance gene. The results showed that the resistance to Pm28 in Ludou 4 and Cangdou 5 was controlled by a single dominant gene Rps9, which was located on the molecular linkage group N between the SSR markers Satt631 （7.5 cM） and Sat_186 （4.3 cM）.展开更多
Plants secrete defense molecules into the extracellular space (the apoplast) to combat attacking microbes. However, the mechanisms by which successful pathogens subvert plant apoplastic immunity remain poorly understo...Plants secrete defense molecules into the extracellular space (the apoplast) to combat attacking microbes. However, the mechanisms by which successful pathogens subvert plant apoplastic immunity remain poorly understood. In this study, we show that PsAvh240, a membrane-localized effector of the soybean pathogen Phytophthora sojae, promotes P. sojae infection in soybean hairy roots. We found that PsAvh240 interacts with the soybean-resistant aspartic protease GmAP1 in planta and suppresses the secretion of GmAP1 into the apoplast. By solving its crystal structure we revealed that PsAvh240 contain six a helices and two WY motifs. The first two a helices of PsAvh240 are responsible for its plasma membrane-localization and are required for PsAvh240's interaction with GmAP1. The second WY motifs of two PsAvh240 molecules form a handshake arrangement resulting in a handshake-like dimer. This dimerization is required for the effector's repression of GmAP1 secretion. Taken together, these data reveal that PsAvh240 localizes at the plasma membrane to interfere with GmAP1 secretion, which represents an effective mechanism by which effector proteins suppress plant apoplastic immunity.展开更多
Our previous studies indicated that tomato miR482b could negatively regulate the resistance of tomato to Phytophthora infestans and the expression of miR482b was decreased after inoculation with P.infestans.However,th...Our previous studies indicated that tomato miR482b could negatively regulate the resistance of tomato to Phytophthora infestans and the expression of miR482b was decreased after inoculation with P.infestans.However,the mechanism by which the accumulation of miR482b is suppressed remains unclear.In this study,we wrote a program to identify 89 long noncoding RNA(lncRNA)-originated endogenous target mimics(eTMs)for 46 miRNAs from our RNA-Seq data.Three tomato lncRNAs,lncRNA23468,lncRNA01308 and lncRNA13262,contained conserved eTM sites for miR482b.When lncRNA23468 was overexpressed in tomato,miR482b expression was significantly decreased,and the expression of the target genes,NBS-LRRs,was significantly increased,resulting in enhanced resistance to P.infestans.Silencing lncRNA23468 in tomato led to the increased accumulation of miR482b and decreased accumulation of NBS-LRRs,as well as reduced resistance to P.infestans.In addition,the accumulation of both miR482b and NBS-LRRs was not significantly changed in tomato plants that overexpressed lncRNA23468 with a mutated eTM site.Based on the VIGS system,a target gene of miR482b,Solyc02g036270.2,was silenced.The disease symptoms of the VIGS-Solyc02g036270.2 tomato plants were in accordance with those of tomato plants in which lncRNA23468 was silenced after inoculation with P.infestans.More severe disease symptoms were found in the modified plants than in the control plants.Our results demonstrate that lncRNAs functioning as eTMs may modulate the effects of miRNAs in tomato and provide insight into how the lncRNA23468-miR482b-NBS-LRR module regulates tomato resistance to P.infestans.展开更多
Tomato is an important horticultural and economic crop cultivated worldwide.As Phytophthora infestans becomes a huge threat to tomato production,it is necessary to study the resistance mechanisms of tomato against P.i...Tomato is an important horticultural and economic crop cultivated worldwide.As Phytophthora infestans becomes a huge threat to tomato production,it is necessary to study the resistance mechanisms of tomato against P.infestans.Our previous research has found that miR482 might be involved in tomato–P.infestans interaction.In this study,miR482b precursor was cloned from Solanum pimpinellifolium“L3708”and miR482b was shown to decrease in abundance in tomato following P.infestans infection.Compared to wild-type tomato plants,tomato plants that overexpressed miR482b displayed more serious disease symptoms after P.infestans infection,with more necrotic cells,longer lesion diameters,and increased P.infestans abundance.Meanwhile,silencing of miR482b was performed by short tandem target mimic(STTM),resulting in enhancement of tomato resistance to P.infestans.Using miRNA and degradome data sets,NBS–LRR disease-resistance genes targeted by miR482b were validated.Negative correlation between the expression of miR482b and its target genes was found in all miR482b-overexpressing and-silencing tomato plants.Our results provide insight into tomato miR482b involved in the response to P.infestans infection,and demonstrate that miR482b–NBS–LRR is an important component in the network of tomato–P.infestans interaction.展开更多
基金This work was supported by the China Agriculture Research System （CARS-09）, the National Natural Science Foundation of China （31125022 and 31561143007）, and the Program of Introducing Talents of Innovative Discipline to Universities （Project 111） from the State Administration of Foreign Experts Affairs （#B18042）.
文摘Phytophthora pathogens secrete a large arsenal of effectors that manipulate host processes to create an environment conducive to pathogen colonization. However, the underlying mechanisms by which Phytophthora effectors manipulate host plant cells still remain largely unclear. In this study, we report that PcAvr3a12, a Phytophthera capsici RXLR effector and a member of the Avr3a effector family, suppresses plant immunity by targeting and inhibiting host plant peptidyl-prolyl cis-trans isomerase （PPlase）. Overexpression of PcAvr3a 12 in Arabidopsis thaliana enhanced plant susceptibility to P. capsici. FKBP15-2, an endoplasmic reticulum （ER）-Iocalized protein, was identified as a host target of PcAvr3a12 during early P. capsici infection. Analyses of A. thaliana T-DNA insertion mutant （fkbp15-2）, RNAi, and overexpression lines consistently showed that FKBP15-2 positively regulates plant immunity in response to Phytophthora infection. FKBP15-2 possesses PPlase activity essential for its contribution to immunity but is directly suppressed by PcAvr3a12. Interestingly, we found that FKBP15-2 is involved in ER stress sensing and is required for ER stress-mediated plant immunity. Taken together, these results suggest that P. capsici deploys an RXLR effector, PcAvr3a12, to facilitate infection by targeting and suppressing a novel ER-Iocalized PPlase, FKBP15-2, which is required for ER stress-mediated plant immunity.
基金supported by the Earmarked Fund for Modern Agro-Industry Technology Research System, China (nyhyzx07-053)the Program for Changjiang Scholars and Innovative Research Team in University, China (PCSIRT)the Research Fund for the Doctoral Program of Higher Education of China (20090097120023)
文摘Phytophthora sojae Kanfman and Gerdemann （P. sojae） is one of the most prevalent pathogens and causes Phytophthora root rot, which limits soybean production worldwide. Development of resistant cultivars is a cost-effective approach to controlling this disease. In this study, 127 soybean germplasm were evaluated for their responses to Phytophthora sojae strain Pm28 using the hypocotyl inoculation technique, and 49 were found resistant to the strain. The hypocotyl of P1, P2, F1, and F2：3 of two crosses of Ludou 4 （resistant）×Youchu 4 （susceptible） and Cangdou 5 （resistant）×Williams （susceptible） were inoculated with Pm28, and were used to analyze the inheritance of resistance. The population derived from the cross of Ludou 4×Youchu 4 was used to map the resistance gene （designated as Rps9） to a linkage group. 932 pairs of SSR primers were used to detect polymorphism, and seven SSR markers were mapped near the resistance gene. The results showed that the resistance to Pm28 in Ludou 4 and Cangdou 5 was controlled by a single dominant gene Rps9, which was located on the molecular linkage group N between the SSR markers Satt631 （7.5 cM） and Sat_186 （4.3 cM）.
基金supported by grants to Yuanchao Wang from the China National Funds for Innovative Research Groups(31721004)the key program of the National Natural Science Foundation of China(31430073)+2 种基金the Chinese Modern Agricultural Industry Technology System(CARS-004-PS14)the National Key R&D Program of China(SQ2018YFD020042)Research in the W.X.laboratory is supported by the Chinese Thousand Talents Plan and the Chinese Academy of Sciences.B.G.is supported by the Postgraduate Research&Practice Innovation Program of Jiangsu Province(KYCX18.0662).
文摘Plants secrete defense molecules into the extracellular space (the apoplast) to combat attacking microbes. However, the mechanisms by which successful pathogens subvert plant apoplastic immunity remain poorly understood. In this study, we show that PsAvh240, a membrane-localized effector of the soybean pathogen Phytophthora sojae, promotes P. sojae infection in soybean hairy roots. We found that PsAvh240 interacts with the soybean-resistant aspartic protease GmAP1 in planta and suppresses the secretion of GmAP1 into the apoplast. By solving its crystal structure we revealed that PsAvh240 contain six a helices and two WY motifs. The first two a helices of PsAvh240 are responsible for its plasma membrane-localization and are required for PsAvh240's interaction with GmAP1. The second WY motifs of two PsAvh240 molecules form a handshake arrangement resulting in a handshake-like dimer. This dimerization is required for the effector's repression of GmAP1 secretion. Taken together, these data reveal that PsAvh240 localizes at the plasma membrane to interfere with GmAP1 secretion, which represents an effective mechanism by which effector proteins suppress plant apoplastic immunity.
基金supported by grants from the National Natural Science Foundation of China(Nos.31471880 and 61472061).
文摘Our previous studies indicated that tomato miR482b could negatively regulate the resistance of tomato to Phytophthora infestans and the expression of miR482b was decreased after inoculation with P.infestans.However,the mechanism by which the accumulation of miR482b is suppressed remains unclear.In this study,we wrote a program to identify 89 long noncoding RNA(lncRNA)-originated endogenous target mimics(eTMs)for 46 miRNAs from our RNA-Seq data.Three tomato lncRNAs,lncRNA23468,lncRNA01308 and lncRNA13262,contained conserved eTM sites for miR482b.When lncRNA23468 was overexpressed in tomato,miR482b expression was significantly decreased,and the expression of the target genes,NBS-LRRs,was significantly increased,resulting in enhanced resistance to P.infestans.Silencing lncRNA23468 in tomato led to the increased accumulation of miR482b and decreased accumulation of NBS-LRRs,as well as reduced resistance to P.infestans.In addition,the accumulation of both miR482b and NBS-LRRs was not significantly changed in tomato plants that overexpressed lncRNA23468 with a mutated eTM site.Based on the VIGS system,a target gene of miR482b,Solyc02g036270.2,was silenced.The disease symptoms of the VIGS-Solyc02g036270.2 tomato plants were in accordance with those of tomato plants in which lncRNA23468 was silenced after inoculation with P.infestans.More severe disease symptoms were found in the modified plants than in the control plants.Our results demonstrate that lncRNAs functioning as eTMs may modulate the effects of miRNAs in tomato and provide insight into how the lncRNA23468-miR482b-NBS-LRR module regulates tomato resistance to P.infestans.
基金This work was supported by Grants from the NFSC(Nos.31471880 and 61472061).
文摘Tomato is an important horticultural and economic crop cultivated worldwide.As Phytophthora infestans becomes a huge threat to tomato production,it is necessary to study the resistance mechanisms of tomato against P.infestans.Our previous research has found that miR482 might be involved in tomato–P.infestans interaction.In this study,miR482b precursor was cloned from Solanum pimpinellifolium“L3708”and miR482b was shown to decrease in abundance in tomato following P.infestans infection.Compared to wild-type tomato plants,tomato plants that overexpressed miR482b displayed more serious disease symptoms after P.infestans infection,with more necrotic cells,longer lesion diameters,and increased P.infestans abundance.Meanwhile,silencing of miR482b was performed by short tandem target mimic(STTM),resulting in enhancement of tomato resistance to P.infestans.Using miRNA and degradome data sets,NBS–LRR disease-resistance genes targeted by miR482b were validated.Negative correlation between the expression of miR482b and its target genes was found in all miR482b-overexpressing and-silencing tomato plants.Our results provide insight into tomato miR482b involved in the response to P.infestans infection,and demonstrate that miR482b–NBS–LRR is an important component in the network of tomato–P.infestans interaction.
