Numerous shallow earthquakes, including 24 th August Amatrice, 26 th October Visso, and 30 th October Norcia earthquakes, ruptured the segments of Mount Vettore-Gorzano fault system in the central Apennines(Italy) in ...Numerous shallow earthquakes, including 24 th August Amatrice, 26 th October Visso, and 30 th October Norcia earthquakes, ruptured the segments of Mount Vettore-Gorzano fault system in the central Apennines(Italy) in 2016. In order to investigate the stress perturbation and triggering patterns among the earthquake sequences, we introduce a more realistic nonplanar coseismic fault geometry model, which improve the rupture model by assimilating relocated aftershocks and the GPS observations. We adopt the seismic slip inversion program of the steepest descent method(SDM) to create the detailed coseismic rupture models and optimize Coulomb Failure Stress model by varying the coefficient of friction and received fault parameters. The results indicate that the nonplanar fault geometry model is more reflective of the deep slip of the coseismic rupture than planar model. As evidenced by the coseismic Coulomb stress changes caused by the three mainshocks at different depth slices, the stress loading mainly distributes on the active fault zones and the stress changes can well explain the spatial distribution of aftershocks. The first large Amatrice mainshock accelerates the occurrence of the Mw 5.9 Visso and Mw 6.6 Norcia earthquakes, with the positive stress changes at the hypocenter exceeding the stress triggering threshold(0.010×10^(6) Pa) and up to 0.015×10^(6) and 0.257×10^(6) Pa, respectively. Furthermore, the Mw 5.9 Visso earthquake as well encourages the occurrence of the Mw 6.6 Norcia event with the increased stress changes of 0.052×10^(6) Pa on the hypocenter. It is concluded that the stress transfer and accumulation play crucial roles on the linkage triggering mechanism among the mainshock-mainshock and mainshockaftershocks. Noteworthily, the cumulative stress changes on the southwest segment of the Norcia Fault(NF), the southeast parts of the Montereale Fault System(MFS) and Mount Gorzano Fault(MGF) of the main regions are up to(1.5~3.5) ×10^(6) Pa. The cumulative stress changes have not been released sufficiently by aftershocks, which may increase the seismic hazard in those regions.展开更多
CRISPR/Cas9-mediated genome engineering technologies are now widely applied in various organisms,including mouse and human cells（Cong et al.,2013;Mali et al.,2013;Yang et al.,2013;Hsu et al.,2014）.The most widely us...CRISPR/Cas9-mediated genome engineering technologies are now widely applied in various organisms,including mouse and human cells（Cong et al.,2013;Mali et al.,2013;Yang et al.,2013;Hsu et al.,2014）.The most widely used customized CRISPR/Cas9（Sp Cas9）is derived from Streptococcus pyogenes（Cong et al.,2013）.展开更多
Dear Editor,To combat pathogen invasion,plants use immune receptors that detect immunogenic molecules to trigger immune responses and confer resistance.Cell-surface-resident pattern recognition receptors activate patt...Dear Editor,To combat pathogen invasion,plants use immune receptors that detect immunogenic molecules to trigger immune responses and confer resistance.Cell-surface-resident pattern recognition receptors activate pattern-triggered immunity through the perception of pathogen-associated molecular patterns(PAMPs),damage-associated molecular patterns,and phytocytokines(PCKs)(Zhou and Zhang,2020;Jones et al.,2024).展开更多
Plants are engaged in a constant battle for survival against pathogens,which triggers a multifaceted immune response characterized by pattern-triggered immunity(PTI)and effector-triggered immunity(ETI)to prevent infec...Plants are engaged in a constant battle for survival against pathogens,which triggers a multifaceted immune response characterized by pattern-triggered immunity(PTI)and effector-triggered immunity(ETI)to prevent infection.These two immune responses operate synergistically to enhance plant immunity.PTI is considered the first line of defense involving the recognition of pathogen-associated molecular patterns(PAMPs)by specific receptors in host cells known as pattern recognition receptors(PRRs),which initiate defense signaling.However,many pathogens often overcome the first line of defense(PTI)and successfully deploy effector proteins to promote virulence and subvert plant immunity,leading to host susceptibility.In the counter-defense,the ETI defense mechanism is activated by triggering resistance(R)genes in plants that usually encode nucleotide-binding-leucine-rich-containing(NLR)proteins.During plant-pathogen interactions,transcriptional reprogramming of defense-related genes such as pathogenesisrelated proteins and generation of reactive oxygen species(ROS)are essential for facilitating programmed cell death at the infected location to inhibit pathogen proliferation.While ROS and PR protein are critical in plant-pathogen interaction,they are not universally required or effective against all pathogens.Hence,plants’multilayer immune layer is encrypted with the compensatory activation of ETI defense response towards the failure of one component of the defense system to maintain robust immunity.展开更多
Pathogen-driven crop losses pose a significant threat to global food security.Plants deploy two primary branches of innate immunity:pathogen-associated molecular pattern-triggered immunity(PTI)and effector-triggered i...Pathogen-driven crop losses pose a significant threat to global food security.Plants deploy two primary branches of innate immunity:pathogen-associated molecular pattern-triggered immunity(PTI)and effector-triggered immunity(ETI)(Yu et al.,2024).While PTI relies on surface-localized pattern recognition receptors,ETI is mediated by intracellular nucleotide-binding leucine-rich repeat receptors(NLRs)that directly or indirectly recognize pathogen effectors,often triggering hypersensitive cell death and systemic resistance(Yu et al.,2024).展开更多
基金This work is funded by Sichuan Science and Technology Program(No.2020GZYZF0010)National Natural Science Foundation of China(No.41374032.No.41704028).
文摘Numerous shallow earthquakes, including 24 th August Amatrice, 26 th October Visso, and 30 th October Norcia earthquakes, ruptured the segments of Mount Vettore-Gorzano fault system in the central Apennines(Italy) in 2016. In order to investigate the stress perturbation and triggering patterns among the earthquake sequences, we introduce a more realistic nonplanar coseismic fault geometry model, which improve the rupture model by assimilating relocated aftershocks and the GPS observations. We adopt the seismic slip inversion program of the steepest descent method(SDM) to create the detailed coseismic rupture models and optimize Coulomb Failure Stress model by varying the coefficient of friction and received fault parameters. The results indicate that the nonplanar fault geometry model is more reflective of the deep slip of the coseismic rupture than planar model. As evidenced by the coseismic Coulomb stress changes caused by the three mainshocks at different depth slices, the stress loading mainly distributes on the active fault zones and the stress changes can well explain the spatial distribution of aftershocks. The first large Amatrice mainshock accelerates the occurrence of the Mw 5.9 Visso and Mw 6.6 Norcia earthquakes, with the positive stress changes at the hypocenter exceeding the stress triggering threshold(0.010×10^(6) Pa) and up to 0.015×10^(6) and 0.257×10^(6) Pa, respectively. Furthermore, the Mw 5.9 Visso earthquake as well encourages the occurrence of the Mw 6.6 Norcia event with the increased stress changes of 0.052×10^(6) Pa on the hypocenter. It is concluded that the stress transfer and accumulation play crucial roles on the linkage triggering mechanism among the mainshock-mainshock and mainshockaftershocks. Noteworthily, the cumulative stress changes on the southwest segment of the Norcia Fault(NF), the southeast parts of the Montereale Fault System(MFS) and Mount Gorzano Fault(MGF) of the main regions are up to(1.5~3.5) ×10^(6) Pa. The cumulative stress changes have not been released sufficiently by aftershocks, which may increase the seismic hazard in those regions.
基金supported by the grants from the Natural Science Foundation of China (No.81201181 to F.G.81473295 and 81670882 to Z.M.S and 81700885 to X.L.G.)+5 种基金Zhejiang Provincial & Ministry of Health research fund for medical sciences (WKJ2013-2-023 to F.G.WKJ-ZJ-1828 to J.Z.Z.and 2016KYA145 to X.L.G.)Science Technology Project of Zhejiang Province (2014C33260 to Z.M.S.and 2017C37176 to F.G.)Eye Hospital at Wenzhou Medical University (YNZD201602 to F.G.)Wenzhou City (Y20160008 to J.Z.Z.)Research Fund for Lin He's Academician Workstation of New Medicine and Clinical Translation (17331209 to C.B.L.)
文摘CRISPR/Cas9-mediated genome engineering technologies are now widely applied in various organisms,including mouse and human cells（Cong et al.,2013;Mali et al.,2013;Yang et al.,2013;Hsu et al.,2014）.The most widely used customized CRISPR/Cas9（Sp Cas9）is derived from Streptococcus pyogenes（Cong et al.,2013）.
基金supported by the National Natural Science Foundation of China(32472567)the Major Basic Research Project of the Shandong Provincial Natural Science Foundation,China(ZR2024ZD07)+1 种基金and the Key R&D Program of Shandong Province,China(2024CXPT072)to S.H.by the Shandong Provincial Natural Science Foundation Youth Program,China(ZR2024MC065)to C.Y.
文摘Dear Editor,To combat pathogen invasion,plants use immune receptors that detect immunogenic molecules to trigger immune responses and confer resistance.Cell-surface-resident pattern recognition receptors activate pattern-triggered immunity through the perception of pathogen-associated molecular patterns(PAMPs),damage-associated molecular patterns,and phytocytokines(PCKs)(Zhou and Zhang,2020;Jones et al.,2024).
基金National Natural Science Foundation of China(32250410314,32250410283,32470342)Natural Science Foundation of Shanghai(24ZR1430100).
文摘Plants are engaged in a constant battle for survival against pathogens,which triggers a multifaceted immune response characterized by pattern-triggered immunity(PTI)and effector-triggered immunity(ETI)to prevent infection.These two immune responses operate synergistically to enhance plant immunity.PTI is considered the first line of defense involving the recognition of pathogen-associated molecular patterns(PAMPs)by specific receptors in host cells known as pattern recognition receptors(PRRs),which initiate defense signaling.However,many pathogens often overcome the first line of defense(PTI)and successfully deploy effector proteins to promote virulence and subvert plant immunity,leading to host susceptibility.In the counter-defense,the ETI defense mechanism is activated by triggering resistance(R)genes in plants that usually encode nucleotide-binding-leucine-rich-containing(NLR)proteins.During plant-pathogen interactions,transcriptional reprogramming of defense-related genes such as pathogenesisrelated proteins and generation of reactive oxygen species(ROS)are essential for facilitating programmed cell death at the infected location to inhibit pathogen proliferation.While ROS and PR protein are critical in plant-pathogen interaction,they are not universally required or effective against all pathogens.Hence,plants’multilayer immune layer is encrypted with the compensatory activation of ETI defense response towards the failure of one component of the defense system to maintain robust immunity.
基金supported by the Beijing Life Science Academy(Key Laboratory)Project(2024400CB0120)the National Key Research and Development Program of China(2021YFD1400400 and 2022YFD1400800)the National Natural Science Foundation of China(32130086,32430085,and 32300123).
文摘Pathogen-driven crop losses pose a significant threat to global food security.Plants deploy two primary branches of innate immunity:pathogen-associated molecular pattern-triggered immunity(PTI)and effector-triggered immunity(ETI)(Yu et al.,2024).While PTI relies on surface-localized pattern recognition receptors,ETI is mediated by intracellular nucleotide-binding leucine-rich repeat receptors(NLRs)that directly or indirectly recognize pathogen effectors,often triggering hypersensitive cell death and systemic resistance(Yu et al.,2024).
